The DOI matches its Crossref record; 208 of the 208 references it cites were found in a registry or an index; none of the 153 sources its claims cite is checked for support yet.
Food reward, hyperphagia, and obesity
Open accessAbstract
Given the unabated obesity problem, there is increasing appreciation of expressions like “my eyes are bigger than my stomach,” and recent studies in rodents and humans suggest that dysregulated brain reward pathways may be contributing not only to drug addiction but also to increased intake of palatable foods and ultimately obesity. After describing recent progress in revealing the neural pathways and mechanisms underlying food reward and the attribution of incentive salience by internal state signals, we analyze the potentially circular relationship between palatable food intake, hyperphagia, and obesity. Are there preexisting individual differences in reward functions at an early age, and could they be responsible for development of obesity later in life? Does repeated exposure to palatable foods set off a cascade of sensitization as in drug and alcohol addiction? Are reward functions altered by secondary effects of the obese state, such as increased signaling through inflammatory, oxidative, and mitochondrial stress pathways? Answering these questions will significantly impact prevention and treatment of obesity and its ensuing comorbidities as well as eating disorders and drug and alcohol addiction.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review argues that food reward (“liking,” “wanting,” and learning) interacts with homeostatic metabolic signals and may contribute to hyperphagia and obesity through preexisting reward differences, addiction-like neuroadaptation to palatable foods, and secondary effects of the obese state. It concludes that evidence remains largely indirect/correlative, with mesolimbic dopamine implicated in “wanting” but still unclear whether over- or under-activity drives hyperphagia.
Key findings
- Food reward is a composite of “liking” (hedonic impact), “wanting” (incentive salience), and learning, with separable brain systems: μ-opioid-mediated “liking” hotspots in nucleus accumbens shell/ventral pallidum, and mesolimbic dopamine for “wanting”; leptin, ghrelin, and insulin modulate these processes.
- Three non-exclusive mechanisms may link reward to obesity: preexisting differences in reward function, repeated palatable-food intake as an escalating addictive process, and obesity-induced changes in reward circuitry; among ~20 major obesity genes, none are directly implicated in reward, and combined effects account for less than ∼5% of human obesity.
- In Wistar rats, a palatable cafeteria diet produced sustained hyperphagia over 40 days and increased lateral hypothalamic self-stimulation threshold in parallel with weight gain; after 14 days of abstinence, reward threshold did not normalize despite hypophagia and ∼10% body weight loss, unlike the relatively rapid ∼48 h normalization seen after cocaine abstinence.
- Obesity/high-fat diet can alter reward: obesity-prone rats on chow or high-fat diet without extra weight gain showed reduced progressive ratio break point for sucrose, amphetamine-induced conditioned place preference, and nucleus accumbens dopamine turnover; leptin-deficient humans showed exaggerated nucleus accumbens activation to food images that was abolished by leptin.
Methods
- Narrative review, not a primary empirical study; it synthesizes rodent, nonhuman primate, and human literature on food reward, hyperphagia, and obesity.
- Data/sample: cited animal models (rats, mice, primates) and human neuroimaging/clinical studies; no new sample or original dataset.
- Main analysis: conceptual synthesis of neural pathways and three hypothesized reward–obesity mechanisms; no meta-analysis or statistical pooling.
Limitations
- The paper states there is “no smoking gun” for a single specific neural pathway or molecule, and it is not yet clear whether over- or under-activity of dopamine signaling is at the origin of hyperphagia or which mesolimbic dopamine projections are specifically involved.
- The paper notes that few studies dissociate preexisting reward differences from secondary effects of the obese state, and that only longitudinal studies in genetically defined populations will provide more conclusive answers; controlled human studies showing long-term effects of palatability on energy balance are few.
- Evident from the text: as a narrative review, conclusions rely heavily on indirect and correlative evidence from heterogeneous animal models and methodologies, without systematic review or meta-analytic quantification.
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Claims the paper makes
85 Not checked yet · 47 Own interpretation
In the paper
“nutrient sensors in the gastrointestinal tract and elsewhere in the body appear to also contribute to the generation of food reward during and after a meal ([153](#B153)).”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
What the sources say
- Not checked yetcites [153] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the preparatory phase, before any oral contact is made with food, reward expectancy plays a pivotal role.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“By forming representations and reward expectancies through processes of learning and memory, these systems likely evolved to engage powerful motivations and drives for guaranteed supply with and ingestion of beneficial foods from a sparse and often hostile environment.”
§ Food reward, hyperphagia, and obesity > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: unclear — It is unclear whether it could be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“the current obesity epidemic is best explained as a mismatch between the modern environment/lifestyle and biological response patterns that evolved in a scarce environment.”
§ Food reward, hyperphagia, and obesity > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Reward expectancy appears to be the main driver to keep focused during this journey.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These systems are directly and primarily involved in the interactions of the modern environment and lifestyle with the human body.”
§ Food reward, hyperphagia, and obesity > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“reward expectancy is perhaps the main factor determining the outcome of this process.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, the decision to pursue this new goal largely depends on expecting but not actually consuming the reward.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“Research suggests that to make this choice, the brain uses representations of reward-expectancy and effort/risk requirement from prior experiences to optimize cost/benefit”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“But even when all taste processing is eliminated by genetic manipulation, mice still learn to prefer sugar over water, suggesting the generation of food reward by processes of glucose utilization ([44](#B44)).”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
What the sources say
- Not checked yetcites [44] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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- It may state two separate claims as one. 44
- Probably not a substantial claim. 8
None of the sources cited for this claim have been checked yet.
In the paper
“Biological traits like strong attraction to food and food cues, slow satiety mechanisms, and high metabolic efficiency, advantageous for survival in a scarce environment, seem now to be our worst enemies when it comes to resisting an abundance of food”
§ Food reward, hyperphagia, and obesity > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Ingestive behavior is not limited to the act of eating, but consists of preparatory, consummatory, and postconsummatory phases”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
What the sources say
- Not checked yetcites [15] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“During eating, immediate, direct pleasure is derived from mainly gustatory and olfactory sensations, driving consumption throughout the meal until satiation signals dominate ([166](#B166)).”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
What the sources say
- Not checked yetcites [166] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Food intake and energy expenditure are thought to be controlled by complex, redundant, and distributed neural systems, likely involving thousands of genes and reflecting the fundamental biological importance of adequate nutrient supply and energy balance”
§ Food reward, hyperphagia, and obesity > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Biological traits like strong attraction to food and food cues, slow satiety mechanisms, and high metabolic efficiency, advantageous for survival in a scarce environment, seem now to be our worst enemies when it comes to resisting an abundance of food”
§ Food reward, hyperphagia, and obesity > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Neural systems activated by thinking about a favorite dish, savoring a candy in the mouth, or leaning back after a satiating meal, are likely very different, although they may contain common elements.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, a variety of sensory stimuli and emotional states or feelings with vastly different temporal profiles make up the rewarding experience of eating, and the underlying neural functions are only beginning to be understood.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > The many pleasures of eating.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Even in *Drosophila*, the taste-specific receptor cells do not directly synapse on motor neurons responsible for the taste-guided behavioral output ([68](#B68)), leaving plenty of opportunities for modulatory influences from other areas of the nervous system.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
What the sources say
- Not checked yetcites [68] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Even in the fruit fly with its primitive nervous system, stimulation of gustatory neurons with sugar activated, while stimulation with a bitter substance inhibited, a pair of motor neurons in the subesophageal ganglion, leading to either vigorous ingestion or rejection ([68](#B68))”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
What the sources say
- Not checked yetcites [68] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, this basic brainstem circuitry appears to be able to recognize the usefulness and perhaps pleasantness of a taste stimulus and initiate appropriate behavioral responses.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In mice with transgenic expression of the receptor for an ordinarily tasteless ligand in either sweet or bitter taste receptor cells, stimulation with the ligand produced either strong attraction or avoidance of sweet solutions, respectively ([197](#B197)).”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
What the sources say
- Not checked yetcites [197] source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The nucleus accumbens shell is thereby part of a neural loop including the lateral hypothalamus and the ventral tegmental area, with orexin neurons playing a key role ([7](#B7), [22](#B22), [77](#B77), [98](#B98), [115](#B115), [125](#B125), [175](#B175), [199](#B199)).”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Perhaps the most important processing step in the translation of such sensory representations into actions is the attribution of what Berridge calls “incentive salience.””
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This mechanism allows a starving animal to know it needs calories or a salt-depleted organism to know it needs salt.”
§ Food reward, hyperphagia, and obesity > Hedonic Consequences of Food > Neural mechanisms of food reward functions: liking and wanting.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“But clearly, leptin receptors are located in other hypothalamic areas such as the ventromedial, dorsomedial, and premammillary nuclei, as well as the lateral and perifornical areas where they likely contribute to leptin's effects on food intake and energy expenditure”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation via the hypothalamus.
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Similarly, subjective pleasantness in humans was coded by neural activity in the medial orbitofrontal cortex as measured by functional MRI (fMRI) and was subject to sensory-specific satiety, a form of reinforcer devaluation”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “liking” through sensory processing, cortical representation, and cognitive controls.
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“other studies demonstrated that such leptin injections decreased dopamine neuron activity and acutely suppressed food intake, while adenoviral knockdown of leptin receptors specifically in the ventral tegmental area (VTA) resulted in increased sucrose preference and sustained palatable food intake ([84](#B84))”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “wanting” through the mesolimbic dopamine system.
What the sources say
- Not checked yetcites [84] source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Also, in normal rats, leptin promotes tyrosine hydroxylase activity and amphetamine-mediated dopamine efflux in the nucleus accumbens”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “wanting” through the mesolimbic dopamine system.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition to midbrain dopamine neurons, orexin neurons project widely within both forebrain and hindbrain. In particular, a hypothalamic-thalamic-striatal loop involving orexin projections to the paraventricular nucleus of the thalamus and cholinergic striatal interneurons ([93](#B93)), and orexin projections to oromotor and autonomic motor areas in the caudal brainstem ([6](#B6)).”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation via the hypothalamus.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“leptin-deficient mice (absence of leptin-receptor signaling) exhibit suppressed rather than increased dopamine neuron activity [as expected from the viral knockdown experiments in rats ([84](#B84))], and leptin-replacement therapy restored normal dopamine neuron activity as well as amphetamine-induced locomotor sensitization ([63](#B63))”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “wanting” through the mesolimbic dopamine system.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In contrast, ghrelin action directly within the VTA appears to activate dopamine neurons, increase accumbens dopamine turnover, and increase food intake”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “wanting” through the mesolimbic dopamine system.
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Both of these weight loss-induced differences were reversed after leptin treatment, suggesting that low leptin sensitizes brain areas responding to food cues.”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “liking” through sensory processing, cortical representation, and cognitive controls.
What the sources say
- Not checked yetcites [142] Rosenbaum M, 2008, J Clin Invest
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It has long been known that electrical stimulation of the lateral hypothalamus elicits food intake and that rats learn quickly to self-administer electrical stimulation”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation via the hypothalamus.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Neural activation in the nucleus accumbens elicited by visual food stimuli is very high in genetically leptin-deficient adolescents and promptly returns to normal levels upon leptin administration”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “liking” through sensory processing, cortical representation, and cognitive controls.
What the sources say
- Not checked yetcites [57] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In rodents, absence of leptin has been shown to increase and addition of leptin to dampen peripheral taste and olfactory sensitivity”
§ Food reward, hyperphagia, and obesity > Metabolic State Modulates Hedonic Processing > Modulation of “liking” through sensory processing, cortical representation, and cognitive controls.
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“In one such study, only about half of male C57/BL6J mice became obese on a palatable high-fat diet ([55](#B55)), but reward functions were not assessed.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
What the sources say
- Not checked yetcites [55] source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The limited information available suggests that repeated sucrose access can upregulate dopamine release ([5](#B5)) and dopamine transporter ([9](#B9)), and change dopamine D1 and D2 receptor availability ([5](#B5), [8](#B8)) in the nucleus accumbens.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is repeated exposure to addictive foods changing reward mechanisms and leading to accelerated development of obesity?
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“There are also plenty of human studies showing acute effects of manipulating palatability, variability, and availability of food ([191](#B191), [192](#B192)), although few controlled studies show long-term effects on energy balance ([120](#B120), [134](#B134)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This hypothesis is supported by numerous studies in animals demonstrating increased intake of palatable foods and development of obesity, so called diet-induced obesity”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Mesolimbic dopamine signaling is also severely suppressed in leptin-deficient *ob/ob* mice and rescued by systemic leptin replacement ([63](#B63)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
What the sources say
- Not checked yetcites [63] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“However, in genetically leptin-deficient humans, neural activity in the nucleus accumbens elicited by viewing pictures of palatable foods was exaggerated in the absence of leptin and abolished after leptin administration ([57](#B57)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
What the sources say
- Not checked yetcites [57] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Preexisting differences could be determined by genetic and epigenetic alterations, and by early life experience through developmental programming.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, because the combined effect of these genes only accounts for less than ∼5% of human obesity, it is very likely that many important genes have not yet been discovered, some of which could operate within the reward system.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These mechanisms are not mutually exclusive, and it is highly likely that a combination of all three is operative in most individuals.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Such differences could exist before the development of obesity or could be secondary to the obese state, but few studies have attempted to dissociate these two mechanisms.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Do genetic and other preexisting differences in reward functions cause obesity?
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For nonsweet palatable foods (typically high-fat foods), there is less convincing evidence for development of dependence ([21](#B21), [31](#B31)), although intermittent access to corn oil can stimulate dopamine release in the nucleus accumbens ([106](#B106)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is repeated exposure to addictive foods changing reward mechanisms and leading to accelerated development of obesity?
What the sources say
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In Wistar rats, exposure to a palatable cafeteria diet led to sustained hyperphagia over 40 days and lateral hypothalamic electrical self-stimulation threshold increased in parallel to body weight gain ([89](#B89)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is repeated exposure to addictive foods changing reward mechanisms and leading to accelerated development of obesity?
What the sources say
- Not checked yetcites [89] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, it seems clear that the obesity-induced internal toxic environment does not stop at the level of the brain, and within the brain does not stop at the reward circuitry.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is the obese state changing reward mechanisms and accelerating the process?
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although there is considerable indirect and correlative evidence for involvement of the reward system in causing obesity in both animals and humans, there is no smoking gun for a single specific neural pathway or molecule.”
§ Food reward, hyperphagia, and obesity > Conclusions and Perspectives
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“As with drug ([71](#B71), [96](#B96), [156](#B156)) and alcohol ([18](#B18), [185](#B185)) addiction, abstinence from sucrose can cause craving and withdrawal symptoms ([5](#B5)), eventually leading to relapse behavior ([72](#B72), [73](#B73)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is repeated exposure to addictive foods changing reward mechanisms and leading to accelerated development of obesity?
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Obesity is associated with dysregulated signaling systems, such as leptin and insulin resistance, as well as increased signaling through proinflammatory cytokines and pathways activated by oxidative and endoplasmatic reticulum stress ([3](#B3)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is the obese state changing reward mechanisms and accelerating the process?
What the sources say
- Not checked yetcites [3] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Obesity and hypertriglyceridemia produce cognitive impairment in mice, including reduced lever pressing for food reward ([59](#B59)), and epidemiological studies show an association of body mass index and risk of Parkinson disease and cognitive decline ([85](#B85)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is the obese state changing reward mechanisms and accelerating the process?
What the sources say
- Not checked yetcites [59] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Obesity clearly is a multifactorial disease with a number of potential causes, but the involvement of recent environmental changes including overabundance of palatable food and little opportunity to work off the extra energy seems undeniable.”
§ Food reward, hyperphagia, and obesity > Conclusions and Perspectives
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Obesity and hypertriglyceridemia produce cognitive impairment in mice, including reduced lever pressing for food reward ([59](#B59)), and epidemiological studies show an association of body mass index and risk of Parkinson disease and cognitive decline ([85](#B85)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is the obese state changing reward mechanisms and accelerating the process?
What the sources say
- Not checked yetcites [85] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This is most likely because the reward system is complex and cannot be easily manipulated with drugs or genetic deletions.”
§ Food reward, hyperphagia, and obesity > Conclusions and Perspectives
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
- Rests on an assumption: The reward system is complex and cannot be easily manipulated with drugs or genetic deletions.
In the paper
“Interestingly, after 14 days of abstinence from the palatable diet, reward threshold did not normalize even though the rats were hypophagic and lost ∼10% body weight ([89](#B89)).”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is repeated exposure to addictive foods changing reward mechanisms and leading to accelerated development of obesity?
What the sources say
- Not checked yetcites [89] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The end effects of these changes are central insulin and leptin resistance and impaired hypothalamic regulation of energy balance, further favoring the development of obesity and in turn, neurodegeneration.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is the obese state changing reward mechanisms and accelerating the process?
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Given these external conditions together with the strong inherent bias of the homeostatic regulatory system to defend against energy depletion more strongly than energy surplus, weight is easily gained but not so easily lost.”
§ Food reward, hyperphagia, and obesity > Conclusions and Perspectives
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The homeostatic regulatory system has a strong inherent bias to defend against energy depletion more strongly than energy surplus.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results suggest that both obesity per se and high-fat diet can cause alterations in mesolimbic dopamine signaling and reward behaviors.”
§ Food reward, hyperphagia, and obesity > Food Reward and Obesity > Is the obese state changing reward mechanisms and accelerating the process?
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
The anatomy, chemistry, and functions of the elaborate neural systems involved in food reward and their interactions with the hypothalamic homeostatic regulator are poorly understood.
“Regrettably, the anatomy, chemistry, and functions of these elaborate neural systems and their interactions with the homeostatic regulator in the hypothalamus are poorly understood.”
The paper relies on this without support.
Dysregulated brain reward pathways may contribute to increased intake of palatable foods and ultimately obesity.
“recent studies in rodents and humans suggest that dysregulated brain reward pathways may be contributing not only to drug addiction but also to increased intake of palatable foods and ultimately obesity.”
The paper relies on this without support.
Eating is typically experienced as pleasurable and rewarding.
“Eating is typically experienced as pleasurable and rewarding”
The paper relies on this without support.
Food is a powerful natural reinforcer that outcompetes most other behaviors, particularly when an individual is metabolically hungry.
“Thus, food is a powerful natural reinforcer that out competes most other behaviors, particularly when an individual is metabolically hungry.”
The paper relies on this without support.
Metabolic hunger increases motivation to find food and to eat.
“It has long been known that metabolic hunger increases motivation to find food and to eat, but the neural mechanisms involved were obscure.”
The paper relies on this without support.
The hypothalamus is the epicenter of homeostatic regulation.
“Given that the hypothalamus was recognized as the epicenter of homeostatic regulation, it was assumed that the metabolic hunger signal originates in this brain area and propagates through neural projections to other areas important for the organization of goal-directed behavior.”
The paper relies on this without support.
There is no hunger center and no pleasure center in the brain.
“Just as there is no hunger center, there is no pleasure center in the brain.”
The paper relies on this without support.
In animals, only the subconscious components of pleasure (core “liking”) and aversion are experimentally accessible.
“In animals, only the subconscious components of pleasure (Berridge's core “liking”) and aversion are experimentally accessible, and one of the few specific test paradigms is measurement of positive and negative orofacial expressions when tasting pleasurable (typically sweet) or aversive stimuli ([11](#B11)).”
The paper relies on this without support.
A general feeling of satisfaction lingers long after meal termination and contributes to the reinforcing power of a meal.
“Rather than the acute pleasure of tasty food in the mouth, there is a general feeling of satisfaction that lingers on long after termination, and most likely contributes to the reinforcing power of a meal.”
The paper relies on this without support.
Leptin and other metabolic signals act on a large number of brain systems.
“However, during the last few years it became increasingly clear that leptin and the plethora of other metabolic signals not only act on the hypothalamus, but on a large number of brain systems.”
The paper relies on this without support.
Not all subjects exposed to the same toxic environment gain weight.
“this simple explanation does not account for the fact that not all subjects exposed to the same toxic environment gain weight.”
The paper relies on this without support.
Environmental pressure pushes the general population to higher food intake and body weight.
“Although environmental pressure undoubtedly pushes the general population to higher food intake and body weight”
The paper relies on this without support.
Obesity-prone rats develop some degree of obesity even on regular chow diet.
“Because obesity-prone rats develop some degree of obesity even on regular chow diet, it is also not clear to what extent the genetic difference depends on availability of palatable diet vs. chow, to be phenotypically expressed (susceptibility genes).”
The paper relies on this without support.
The homeostatic regulatory system has a strong inherent bias to defend against energy depletion more strongly than energy surplus.
“Given these external conditions together with the strong inherent bias of the homeostatic regulatory system to defend against energy depletion more strongly than energy surplus, weight is easily gained but not so easily lost.”
The paper relies on this without support.
The reward system is complex and cannot be easily manipulated with drugs or genetic deletions.
“This is most likely because the reward system is complex and cannot be easily manipulated with drugs or genetic deletions.”
The paper relies on this without support.
The concept of food addiction is still not generally accepted, and its behavioral and neurological mechanisms remain obscure.
“While the field of drug addiction has a long tradition (e.g., Refs. [96](#B96), [132](#B132)), the concept of food addiction is still not generally accepted, and its behavioral and neurological mechanisms remain obscure.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Ingestive behavior is not only regulated homeostatically (i.e., by central nervous pathways that respond to energy depletion) but also by nonhomeostatic brain circuits that process the reward-related, “hedonic” qualities of food intake (19).”
From Oxytocin Reduces Reward-Driven Food Intake in Humans (2013) · cites this paper as [19]
Citations
Cites
‘Small Changes' to Diet and Physical Activity Behaviors for Weight Management
Hills, A. P., Byrne, N. M., Lindstrom, R. C., & Hill, J. O. (2013) · Obesity Facts · doi:10.1159/000345030 · Cited by 9,526
A neural substrate of prediction and reward
Schultz, W., Dayan, P., & Montague, P. R. (1997) · Science · doi:10.1126/science.275.5306.1593 · Cited by 9,388
Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies
Lang, U. E., & Borgwardt, S. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350094 · Cited by 8,526
Genetics of Food Intake Self-Regulation in Childhood: Literature Review and Research Opportunities
Faith, M. S., Carnell, S., & Kral, T. V. E. (2013) · Human Heredity · doi:10.1159/000353879 · Cited by 7,633
Central nervous system control of food intake
Schwartz, M. W., Woods, S. C., Porte, D., Seeley, R. J., & Baskin, D. G. (2000) · Nature · doi:10.1038/35007534 · Cited by 6,451
Neurons containing hypocretin (orexin) project to multiple neuronal systems
Peyron, C., Tighe, D. K., van den Pol, A. N., de Lecea, L., Heller, H. C., Sutcliffe, J. G., & Kilduff, T. S. (1998) · The Journal of Neuroscience · doi:10.1523/jneurosci.18-23-09996.1998 · Cited by 3,466
Watterson, K. R., Bestow, D., Gallagher, J. R., Hamilton, D. L., Ashford, F. B., Meakin, P. J., & Ashford, M. L. J. (2012) · Neurosignals · doi:10.1159/000334144 · Cited by 3,395
NEURAL MECHANISMS OF ADDICTION: The Role of Reward-Related Learning and Memory
Hyman, S. E., Malenka, R. C., & Nestler, E. J. (2006) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.29.051605.113009 · Cited by 2,647
From motivation to action: Functional interface between the limbic system and the motor system
MOGENSON, G., JONES, D., & YIM, C. (1980) · Progress in Neurobiology · doi:10.1016/0301-0082(80)90018-0 · Cited by 2,331
Food reward: brain substrates of wanting and liking
Berridge, K. C. (1996) · Neuroscience & Biobehavioral Reviews · doi:10.1016/0149-7634(95)00033-b · Cited by 1,901
Berridge, K. C., & Robinson, T. E. (2003) · Trends in Neurosciences · doi:10.1016/s0166-2236(03)00233-9 · Cited by 1,869
The Orbitofrontal Cortex and Reward
Rolls, E. T. (2000) · Cerebral Cortex · doi:10.1093/cercor/10.3.284 · Cited by 1,595
Bunney, W. E., Hippius, H., Laakmann, G., & Schmauß, M. (1990) · Springer eBooks · doi:10.1007/978-3-642-74034-3 · Cited by 1,523
The psychology and neurobiology of addiction: an incentive–sensitization view
Robinson, T. E., & Berridge, K. C. (2000) · Addiction · doi:10.1046/j.1360-0443.95.8s2.19.x · Cited by 1,507
The Neuroscience of Natural Rewards: Relevance to Addictive Drugs
Kelley, A. E., & Berridge, K. C. (2002) · Journal of Neuroscience · doi:10.1523/jneurosci.22-09-03306.2002 · Cited by 1,505
Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats
Johnson, P. M., & Kenny, P. J. (2010) · Nature Neuroscience · doi:10.1038/nn.2519 · Cited by 1,495
Addiction and the brain antireward system
Koob, G. F., & Le Moal, M. (2008) · Annual Review of Psychology · doi:10.1146/annurev.psych.59.103006.093548 · Cited by 1,457
Avena, N. M., Rada, P., & Hoebel, B. G. (2008) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2007.04.019 · Cited by 1,358
Hypothalamic IKKβ/NF-κB and ER Stress Link Overnutrition to Energy Imbalance and Obesity
Zhang, X., Zhang, G., Zhang, H., Karin, M., Bai, H., & Cai, D. (2008) · Cell · doi:10.1016/j.cell.2008.07.043 · Cited by 1,350
A role for lateral hypothalamic orexin neurons in reward seeking
Harris, G. C., Wimmer, M., & Aston-Jones, G. (2005) · Nature · doi:10.1038/nature04071 · Cited by 1,311
Affective neuroscience of pleasure: reward in humans and animals
Berridge, K. C., & Kringelbach, M. L. (2008) · Psychopharmacology · doi:10.1007/s00213-008-1099-6 · Cited by 1,254
Nucleus accumbens D2/3 receptors predict trait impulsivity and cocaine reinforcement
Dalley, J. W., Fryer, T. D., Brichard, L., Robinson, E. S. J., Theobald, D. E. H., Lääne, K., Peña, Y., Murphy, E. R., Shah, Y., Probst, K., et al. (2007) · Science · doi:10.1126/science.1137073 · Cited by 1,188
De Souza, C. T., Araujo, E. P., Bordin, S., Ashimine, R., Zollner, R. L., Boschero, A. C., Saad, M. J. A., & Velloso, L. A. (2005) · Endocrinology · doi:10.1210/en.2004-1520 · Cited by 1,171
Alzheimer’s disease is type 3 diabetes—Evidence reviewed
de la Monte, S. M., & Wands, J. R. (2008) · Journal of Diabetes Science and Technology · doi:10.1177/193229680800200619 · Cited by 1,158
Saper, C. B., Chou, T. C., & Elmquist, J. K. (2002) · Neuron · doi:10.1016/s0896-6273(02)00969-8 · Cited by 1,120
The Human Obesity Gene Map: The 2005 Update
Rankinen, T., Zuberi, A., Chagnon, Y. C., Weisnagel, S. J., Argyropoulos, G., Walts, B., Pérusse, L., & Bouchard, C. (2006) · Obesity · doi:10.1038/oby.2006.71 · Cited by 1,119
How can drug addiction help us understand obesity?
Volkow, N. D., & Wise, R. A. (2005) · Nature Neuroscience · doi:10.1038/nn1452 · Cited by 1,089
Incubation of cocaine craving after withdrawal
Grimm, J. W., Hope, B. T., Wise, R. A., & Shaham, Y. (2001) · Nature · doi:10.1038/35084134 · Cited by 1,031
Gluckman, P. D., Hanson, M. A., & Beedle, A. S. (2007) · American Journal of Human Biology · doi:10.1002/ajhb.20590 · Cited by 1,006
Blum, K., Braverman, E. R., Holder, J. M., Lubar, J. F., Monastra, V. J., Miller, D., Lubar, J. O., Chen, T. J. H., & Comings, D. E. (2000) · Journal of Psychoactive Drugs · doi:10.1080/02791072.2000.10736099 · Cited by 998
Abizaid, A., Liu, Z.-W., Andrews, Z. B., Shanabrough, M., Borok, E., Elsworth, J. D., Roth, R. H., Sleeman, M. W., Picciotto, M. R., Tschöp, M. H., et al. (2006) · Journal of Clinical Investigation · doi:10.1172/jci29867 · Cited by 984 · cited 3×
“Altered reward functions could cause obesity via increased intake of calories or fat (1), or alternatively, could result from consequences of the obese state (3), or could be a combination of both.”
BackgroundPlasticity of reward neurocircuitry and the ‘dark side’ of drug addiction
Koob, G. F., & Le Moal, M. (2005) · Nature Neuroscience · doi:10.1038/nn1105-1442 · Cited by 963
Temporal Prediction Errors in a Passive Learning Task Activate Human Striatum
McClure, S. M., Berns, G. S., & Montague, P. R. (2003) · Neuron · doi:10.1016/s0896-6273(03)00154-5 · Cited by 917
Leptin Receptor Signaling in Midbrain Dopamine Neurons Regulates Feeding
Hommel, J. D., Trinko, R., Sears, R. M., Georgescu, D., Liu, Z.-W., Gao, X.-B., Thurmon, J. J., Marinelli, M., & DiLeone, R. J. (2006) · Neuron · doi:10.1016/j.neuron.2006.08.023 · Cited by 902
Sensory specific satiety in man☆
Rolls, B. J., Rolls, E. T., Rowe, E. A., & Sweeney, K. F. (1981) · Physiology & Behavior · doi:10.1016/0031-9384(81)90310-3 · Cited by 884
Endoplasmic Reticulum Stress Plays a Central Role in Development of Leptin Resistance
Ozcan, L., Ergin, A. S., Lu, A., Chung, J., Sarkar, S., Nie, D., Myers, M. G., & Ozcan, U. (2009) · Cell Metabolism · doi:10.1016/j.cmet.2008.12.004 · Cited by 875
The tempted brain eats: Pleasure and desire circuits in obesity and eating disorders
Berridge, K. C., Ho, C.-Y., Richard, J. M., & DiFeliceantonio, A. G. (2010) · Brain Research · doi:10.1016/j.brainres.2010.04.003 · Cited by 873
Common sense about taste: from mammals to insects
Yarmolinsky, D. A., Zuker, C. S., & Ryba, N. J. P. (2009) · Cell · doi:10.1016/j.cell.2009.10.001 · Cited by 856
Reward, Motivation, and Reinforcement Learning
Dayan, P., & Balleine, B. W. (2002) · Neuron · doi:10.1016/s0896-6273(02)00963-7 · Cited by 855
Ghrelin controls hippocampal spine synapse density and memory performance
Diano, S., Farr, S. A., Benoit, S. C., McNay, E. C., da Silva, I., Horvath, B., Gaskin, F. S., Nonaka, N., Jaeger, L. B., Banks, W. A., et al. (2006) · Nature Neuroscience · doi:10.1038/nn1656 · Cited by 828
Kringelbach, M. L. (2003) · Cerebral Cortex · doi:10.1093/cercor/13.10.1064 · Cited by 824
Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology
Volkow, N. D., Wang, G.-J., Fowler, J. S., & Telang, F. (2008) · Philosophical Transactions of the Royal Society B: Biological Sciences · doi:10.1098/rstb.2008.0107 · Cited by 809
Portion size of food affects energy intake in normal-weight and overweight men and women
Rolls, B. J., Morris, E. L., & Roe, L. S. (2002) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/76.6.1207 · Cited by 793
Hare, T. A., O'Doherty, J., Camerer, C. F., Schultz, W., & Rangel, A. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.1309-08.2008 · Cited by 792
Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by Taq IA A1 Allele
Stice, E., Spoor, S., Bohon, C., & Small, D. M. (2008) · Science · doi:10.1126/science.1161550 · Cited by 786
Stice, E., Spoor, S., Bohon, C., Veldhuizen, M. G., & Small, D. M. (2008) · Journal of Abnormal Psychology · doi:10.1037/a0013600 · Cited by 779
Wyvell, C. L., & Berridge, K. C. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-21-08122.2000 · Cited by 764 · cited 1×
“Recent investigations show that lateral hypothalamic neurons expressing orexin (77, 199) and other transmitters such as neurotensin (101, 107) provide modulatory input to midbrain dopamine neurons well known to be crucial players in translating motivation into action (10, 14, 22, 42, 77, 91, 148, 194, 196).”
BackgroundNeural synchrony in cortical networks: history, concept and current status
Uhlhaas, P. (2009) · Frontiers in Integrative Neuroscience · doi:10.3389/neuro.07.017.2009 · Cited by 758
Multiple neural systems controlling food intake and body weight
Berthoud, H.-R. (2002) · Neuroscience & Biobehavioral Reviews · doi:10.1016/s0149-7634(02)00014-3 · Cited by 725
Self-citationBerridge, K. (2000) · Neuroscience & Biobehavioral Reviews · doi:10.1016/s0149-7634(99)00072-x · Cited by 721
Borgland, S. L., Taha, S. A., Sarti, F., Fields, H. L., & Bonci, A. (2006) · Neuron · doi:10.1016/j.neuron.2006.01.016 · Cited by 718
Ghrelin Modulates Brain Activity in Areas that Control Appetitive Behavior
Malik, S., McGlone, F., Bedrossian, D., & Dagher, A. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.03.007 · Cited by 677
Peciña, S., & Berridge, K. C. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.2329-05.2005 · Cited by 671
The addicted synapse: mechanisms of synaptic and structural plasticity in nucleus accumbens
Russo, S. J., Dietz, D. M., Dumitriu, D., Morrison, J. H., Malenka, R. C., & Nestler, E. J. (2010) · Trends in Neurosciences · doi:10.1016/j.tins.2010.02.002 · Cited by 654
Leptin Regulation of the Mesoaccumbens Dopamine Pathway
Fulton, S., Pissios, P., Manchon, R. P., Stiles, L., Frank, L., Pothos, E. N., Maratos-Flier, E., & Flier, J. S. (2006) · Neuron · doi:10.1016/j.neuron.2006.09.006 · Cited by 644
De Araujo, I. E. T., Rolls, E. T., Kringelbach, M. L., McGlone, F., & Phillips, N. (2003) · European Journal of Neuroscience · doi:10.1046/j.1460-9568.2003.02915.x · Cited by 642
Leptin Regulates Striatal Regions and Human Eating Behavior
Farooqi, I. S., Bullmore, E., Keogh, J., Gillard, J., O'Rahilly, S., & Fletcher, P. C. (2007) · Science · doi:10.1126/science.1144599 · Cited by 622
Dietary obesity in adult rats: Similarities to hypothalamic and human obesity syndromes
Sclafani, A. J., & Springer, D. (1976) · Physiology & Behavior · doi:10.1016/0031-9384(76)90109-8 · Cited by 616
The arcuate nucleus as a conduit for diverse signals relevant to energy homeostasis
Cone, R. D., Cowley, M. A., Butler, A. A., Fan, W., Dl, M., & Low, M. J. (2001) · International Journal of Obesity · doi:10.1038/sj.ijo.0801913 · Cited by 591
Effect of sensory perception of foods on appetite and food intake: a review of studies on humans
Sørensen, L. B., Møller, P., Flint, A., Martens, M., & Raben, A. (2003) · International Journal of Obesity · doi:10.1038/sj.ijo.0802391 · Cited by 589
Grill, H. J., & Norgren, R. (1978) · Brain Research · doi:10.1016/0006-8993(78)90569-3 · Cited by 588
Posey, K. A., Clegg, D. J., Printz, R. L., Byun, J., Morton, G. J., Vivekanandan-Giri, A., Pennathur, S., Baskin, D. G., Heinecke, J. W., Woods, S. C., et al. (2009) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90377.2008 · Cited by 586
Neuropharmacology of alcohol addiction
Vengeliene, V., Bilbao, A., Molander, A., & Spanagel, R. (2008) · British Journal of Pharmacology · doi:10.1038/bjp.2008.30 · Cited by 585
Farooqi, I. S., & O’Rahilly, S. (2006) · Endocrine Reviews · doi:10.1210/er.2006-0040 · Cited by 583
Excitation of Ventral Tegmental Area Dopaminergic and Nondopaminergic Neurons by Orexins/Hypocretins
Korotkova, T. M., Sergeeva, O. A., Eriksson, K. S., Haas, H. L., & Brown, R. E. (2003) · Journal of Neuroscience · doi:10.1523/jneurosci.23-01-00007.2003 · Cited by 583
Erratum to: “Parsing reward” [Trends Neurosci. 26 (2003) 507–513]
Berridge, K. C., & Robinson, T. E. (2003) · Trends in Neurosciences · doi:10.1016/j.tins.2003.09.001 · Cited by 562
Diet-Induced Obesity Causes Severe but Reversible Leptin Resistance in Arcuate Melanocortin Neurons
Enriori, P. J., Evans, A. E., Sinnayah, P., Jobst, E. E., Tonelli-Lemos, L., Billes, S. K., Glavas, M. M., Grayson, B. E., Perello, M., Nillni, E. A., et al. (2007) · Cell Metabolism · doi:10.1016/j.cmet.2007.02.004 · Cited by 552
Motor control in a Drosophila taste circuit
Gordon, M. D., & Scott, K. (2009) · Neuron · doi:10.1016/j.neuron.2008.12.033 · Cited by 531
Compulsive overeating as an addiction disorder. A review of theory and evidence
Davis, C. A., & Carter, J. C. (2009) · Appetite · doi:10.1016/j.appet.2009.05.018 · Cited by 526
The receptors and coding logic for bitter taste
Mueller, K. L., Hoon, M. A., Erlenbach, I., Chandrashekar, J., Zuker, C. S., & Ryba, N. J. P. (2005) · Nature · doi:10.1038/nature03352 · Cited by 524
Postcocaine anhedonia. An animal model of cocaine withdrawal.
Markou, A., & Koob, G. F. (1991) · PubMed · Cited by 505
Wang, G.-J., Volkow, N. D., Thanos, P. K., & Fowler, J. S. (2004) · Journal of Addictive Diseases · doi:10.1300/j069v23n03_04 · Cited by 502
Cellular neuroadaptations to chronic opioids: tolerance, withdrawal and addiction
Christie, M. J. (2008) · British Journal of Pharmacology · doi:10.1038/bjp.2008.100 · Cited by 493
Kleinridders, A., Schenten, D., Könner, A. C., Belgardt, B. F., Mauer, J., Okamura, T., Wunderlich, F. T., Medzhitov, R., & Brüning, J. C. (2009) · Cell Metabolism · doi:10.1016/j.cmet.2009.08.013 · Cited by 483
Sensory-specific satiety-related olfactory activation of the human orbitofrontal cortex
OʼDoherty, J., Rolls, E. T., Francis, S., Bowtell, R., McGlone, F., Kobal, G., Renner, B., & Ahne, G. (2000) · NeuroReport · doi:10.1097/00001756-200002070-00035 · Cited by 482
Rolls, E. T., Sienkiewicz, Z. J., & Yaxley, S. (1989) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.1989.tb00774.x · Cited by 466
Oral sucrose stimulation increases accumbens dopamine in the rat
Hajnal, A., Smith, G. P., & Norgren, R. (2004) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00282.2003 · Cited by 449
Impairment of long-term potentiation and spatial memory in leptin receptor-deficient rodents
Li, X.-L., Aou, S., Oomura, Y., Hori, N., Fukunaga, K., & Hori, T. (2002) · Neuroscience · doi:10.1016/s0306-4522(02)00162-8 · Cited by 440
Jerlhag, E., Egecioglu, E., Dickson, S. L., Douhan, A., Svensson, L., & Engel, J. A. (2007) · Addiction Biology · doi:10.1111/j.1369-1600.2006.00041.x · Cited by 431
Human cortical gustatory areas: A review of functional neuroimaging data
Small, D. M., Zald, D. H., Jones-Gotman, M., Zatorre, R. J., Pardo, J. V., Frey, S., & Petrides, M. (1999) · NeuroReport · doi:10.1097/00001756-199901180-00002 · Cited by 431
Food Reward in the Absence of Taste Receptor Signaling
de Araujo, I. E., Oliveira-Maia, A. J., Sotnikova, T. D., Gainetdinov, R. R., Caron, M. G., Nicolelis, M. A. L., & Simon, S. A. (2008) · Neuron · doi:10.1016/j.neuron.2008.01.032 · Cited by 431
Fisher, J. O., Rolls, B. J., & Birch, L. L. (2003) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/77.5.1164 · Cited by 431
Modulation of Brain Reward Circuitry by Leptin
Fulton, S. E., Woodside, B. C., & Shizgal, P. (2000) · Science · doi:10.1126/science.287.5450.125 · Cited by 421
Leinninger, G. M., Jo, Y.-H., Leshan, R. L., Louis, G. W., Yang, H., Barrera, J. G., Wilson, H., Opland, D. M., Faouzi, M. A., Gong, Y., et al. (2009) · Cell Metabolism · doi:10.1016/j.cmet.2009.06.011 · Cited by 412
Naleid, A. M., Grace, M. K., Cummings, D. E., & Levine, A. S. (2005) · Peptides · doi:10.1016/j.peptides.2005.04.025 · Cited by 409
ROSENBAUM, M. S., Sy, M., Pavlovich, K. H., Leibel, R. L., & Joy Hirsch, C. (2008) · Journal of Clinical Investigation · doi:10.1172/jci35055 · Cited by 408
Vuilleumier, P., & Driver, J. (2007) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2007.2092 · Cited by 397
Insulin resistance and Alzheimer's disease
De La Monte, S. M. (2009) · BMB Reports · doi:10.5483/bmbrep.2009.42.8.475 · Cited by 392
Hypothalamic Control of Feeding and Self-Stimulation
Hoebel, B. G., & Teitelbaum, P. (1962) · Science · doi:10.1126/science.135.3501.375 · Cited by 389
Neurobiological evidence for hedonic allostasis associated with escalating cocaine use
Ahmed, S. H., Kenny, P. J., Koob, G. F., & Markou, A. (2002) · Nature Neuroscience · doi:10.1038/nn872 · Cited by 389
Obesity and Hypertriglyceridemia Produce Cognitive Impairment
Farr, S. A., Yamada, K. A., Butterfield, D. A., Abdul, H. M., Xu, L., Miller, N. E., Banks, W. A., & Morley, J. E. (2008) · Endocrinology · doi:10.1210/en.2007-1722 · Cited by 382
Speakman, J. R. (2008) · International Journal of Obesity · doi:10.1038/ijo.2008.161 · Cited by 361
Sensory-specific satiety-related olfactory activation of the human orbitofrontal cortex
OʼDoherty, J., Rolls, E. T., Francis, S., Bowtell, R., McGlone, F., Kobal, G., Renner, B., & Ahne, G. (2000) · NeuroReport · doi:10.1097/00001756-200003200-00046 · Cited by 361
Feeding and hypothalamic stimulation increase dopamine turnover in the accumbens
Hernandez, L., & Hoebel, B. G. (1988) · Physiology & Behavior · doi:10.1016/0031-9384(88)90324-1 · Cited by 355
Nakamura, T., Uramura, K., Nambu, T., Yada, T., Goto, K., Yanagisawa, M., & Sakurai, T. (2000) · Brain Research · doi:10.1016/s0006-8993(00)02555-5 · Cited by 352
Kelley, A. E., Baldo, B. A., & Pratt, W. E. (2005) · Journal of Comparative Neurology · doi:10.1002/cne.20769 · Cited by 352
Food Craving and Food “Addiction”
Rogers, P. J., & Smit, H. J. (2000) · Pharmacology Biochemistry and Behavior · doi:10.1016/s0091-3057(00)00197-0 · Cited by 347
Central and Peripheral Regulation of Food Intake and Physical Activity: Pathways and Genes
Lenard, N. R., & Berthoud, H. (2008) · Obesity · doi:10.1038/oby.2008.511 · Cited by 338
Self-citationBad Popcorn in Big Buckets: Portion Size Can Influence Intake as Much as Taste
Wansink, B., & Kim, J. (2005) · Journal of Nutrition Education and Behavior · doi:10.1016/s1499-4046(06)60278-9 · Cited by 322
O'Doherty, J. P., Buchanan, T. W., Seymour, B., & Dolan, R. J. (2006) · Neuron · doi:10.1016/j.neuron.2005.11.014 · Cited by 322
Stratford, T. R., & Kelley, A. E. (1999) · Journal of Neuroscience · doi:10.1523/jneurosci.19-24-11040.1999 · Cited by 316
Davis, C. A., Levitan, R. D., Reid, C., Carter, J. C., Kaplan, A. S., Patte, K. A., King, N., Curtis, C., & Kennedy, J. L. (2009) · Obesity · doi:10.1038/oby.2009.52 · Cited by 314
Forebrain substrates of reward and motivation
Wise, R. A. (2005) · The Journal of Comparative Neurology · doi:10.1002/cne.20689 · Cited by 309
Davis, J. F., Tracy, A. L., Schurdak, J. D., Tschöp, M. H., Lipton, J. W., Clegg, D. J., & Benoit, S. C. (2008) · Behavioral Neuroscience · doi:10.1037/a0013111 · Cited by 307
Relation of obesity to consummatory and anticipatory food reward
Stice, E. M., Spoor, S. T. P., Ng, J., & Zald, D. H. (2009) · Physiology & Behavior · doi:10.1016/j.physbeh.2009.03.020 · Cited by 306
Wansink, B., van Ittersum, K., & Painter, J. E. (2006) · American Journal of Preventive Medicine · doi:10.1016/j.amepre.2006.04.003 · Cited by 301
Covert expectation-of-reward in rat ventral striatum at decision points
van der Meer, M. A. A. (2009) · Frontiers in Integrative Neuroscience · doi:10.3389/neuro.07.001.2009 · Cited by 299
Pelchat, M. L. (2002) · Physiology & Behavior · doi:10.1016/s0031-9384(02)00757-6 · Cited by 284
Responses to the Sensory Properties of Fat of Neurons in the Primate Orbitofrontal Cortex
Rolls, E. T., Critchley, H. D., Browning, A. S., Hernadi, I., & Lenard, L. (1999) · The Journal of Neuroscience · doi:10.1523/jneurosci.19-04-01532.1999 · Cited by 278
Sweet taste signaling functions as a hypothalamic glucose sensor
Ren, X. (2009) · Frontiers in Integrative Neuroscience · doi:10.3389/neuro.07.012.2009 · Cited by 267
Neural substrates of conditioned-cued relapse to drug-seeking behavior
See, R. E. (2002) · Pharmacology Biochemistry and Behavior · doi:10.1016/s0091-3057(01)00682-7 · Cited by 264
Cerebral processing of food-related stimuli: effects of fasting and gender
Uher, R., Treasure, J., Heining, M., Brammer, M. J., & Campbell, I. C. (2006) · Behavioural Brain Research · doi:10.1016/j.bbr.2005.12.008 · Cited by 258
Carbohydrate taste, appetite, and obesity: An overview
Sclafani, A. (1987) · Neuroscience & Biobehavioral Reviews · doi:10.1016/s0149-7634(87)80019-2 · Cited by 255
Representation of Umami Taste in the Human Brain
de Araujo, I. E. T., Kringelbach, M. L., Rolls, E. T., & Hobden, P. (2003) · Journal of Neurophysiology · doi:10.1152/jn.00669.2002 · Cited by 254
Rolls, E. T., McCabe, C., & Redouté, J. (2007) · Cerebral Cortex · doi:10.1093/cercor/bhm097 · Cited by 251
Hypothalamic pathways underlying the endocrine, autonomic, and behavioral effects of leptin
Elmquist, J. K. (2001) · Physiology & Behavior · doi:10.1016/s0031-9384(01)00613-8 · Cited by 249
Zheng, H., Patterson, L. M., & Berthoud, H.-R. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.3542-07.2007 · Cited by 248
Self-citationSpeakman, J. R. (2007) · Cell Metabolism · doi:10.1016/j.cmet.2007.06.004 · Cited by 242
Food for thought: hedonic experience beyond homeostasis in the human brain
Kringelbach, M. L. (2004) · Neuroscience · doi:10.1016/j.neuroscience.2004.04.035 · Cited by 236
The direct and indirect controls of meal size
Smith, G. P. (1996) · Neuroscience & Biobehavioral Reviews · doi:10.1016/0149-7634(95)00038-g · Cited by 234
Perinatal Programming and Functional Teratogenesis: Impact on Body Weight Regulation and Obesity
PLAGEMANN, A. (2005) · Physiology & Behavior · doi:10.1016/j.physbeh.2005.08.065 · Cited by 233
Luxuskonsumption, diet-induced thermogenesis and brown fat: the case in favour
Rothwell, N. J., & Stock, M. J. (1983) · Clinical Science · doi:10.1042/cs0640019 · Cited by 229
Developmental programming of hypothalamic feeding circuits
Bouret, S., & Simerly, R. (2006) · Clinical Genetics · doi:10.1111/j.1399-0004.2006.00684.x · Cited by 227
Adiposity signals and food reward: expanding the CNS roles of insulin and leptin
Figlewicz, D. P. (2003) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00602.2002 · Cited by 221
Immunohistochemical localization of leptin receptor in the rat brain
Shioda, S., Funahashi, H., Nakajo, S., Yada, T., Maruta, O., & Nakai, Y. (1998) · Neuroscience Letters · doi:10.1016/s0304-3940(98)00082-2 · Cited by 219
Physiologic Programming of the Fetus
Seckl, J. R. (1998) · Clinics in Perinatology · doi:10.1016/s0095-5108(18)30091-5 · Cited by 210
Hypoglycemia Activates Orexin Neurons and Selectively Increases Hypothalamic Orexin-B Levels
Cai, X. J., Evans, M. L., Lister, C. A., Leslie, R. A., Arch, J. R. S., Wilson, S., & Williams, G. (2001) · Diabetes · doi:10.2337/diabetes.50.1.105 · Cited by 206
Taste receptor signaling in the mammalian gut
Rozengurt, E., & Sternini, C. (2007) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2007.10.002 · Cited by 203
Body mass index and the risk of Parkinson disease
Hu, G., Jousilahti, P., Nissinen, A., Antikainen, R., Kivipelto, M., & Tuomilehto, J. (2006) · Neurology · doi:10.1212/01.wnl.0000247052.18422.e5 · Cited by 203
Leptin and its role in hippocampal synaptic plasticity
HARVEY, J., SOLOVYOVA, N., & IRVING, A. (2006) · Progress in Lipid Research · doi:10.1016/j.plipres.2006.03.001 · Cited by 202
Reward sensitivity and the D2 dopamine receptor gene: A case-control study of binge eating disorder
Davis, C., Levitan, R. D., Kaplan, A. S., Carter, J., Reid, C., Curtis, C., Patte, K., Hwang, R., & Kennedy, J. L. (2008) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2007.09.024 · Cited by 200
Obesity and vulnerability of the CNS
Bruce-Keller, A. J., Keller, J. N., & Morrison, C. D. (2009) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2008.10.004 · Cited by 200 · cited 1×
“It is becoming clear that the obesity-induced toxic internal environment does not spare the brain (24, 46, 48, 52, 59, 95, 121, 127, 177, 182, 198).”
BackgroundLeptin Modulates Behavioral Responses to Sweet Substances by Influencing Peripheral Taste Structures
Shigemura, N., Ohta, R., Kusakabe, Y., Miura, H., Hino, A., Koyano, K., Nakashima, K., & Ninomiya, Y. (2004) · Endocrinology · doi:10.1210/en.2003-0602 · Cited by 199
The Brain as a Target for Inflammatory Processes and Neuroprotective Strategies
Skaper, S. D. (2007) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1403.002 · Cited by 194
Evidence for defective mesolimbic dopamine exocytosis in obesity‐prone rats
Geiger, B. M., Behr, G. G., Frank, L. E., Caldera-Siu, A. D., Beinfeld, M. C., Kokkotou, E. G., & Pothos, E. N. (2008) · The FASEB Journal · doi:10.1096/fj.08-110759 · Cited by 194
Schmid, D. A., Held, K., Ising, M., Uhr, M., Weikel, J. C., & Steiger, A. (2005) · Neuropsychopharmacology · doi:10.1038/sj.npp.1300670 · Cited by 181 · cited 1×
“Furthermore, neural activity in brain areas thought to be involved in cognitive processing of representations of food such as the amygdala and hippocampal complex is modulated by leptin (78, 79, 105) and ghrelin (27, 50, 92, 109, 147, 189).”
BackgroundOrganization of orosensory responses in the nucleus of the solitary tract of rat
Travers, S. P., & Norgren, R. (1995) · Journal of Neurophysiology · doi:10.1152/jn.1995.73.6.2144 · Cited by 179 · cited 1×
“In mammals, the caudal brainstem is the equivalent of the subesophageal ganglion, where direct sensory feedback from the tongue and the gut are integrated into basic motor patterns of ingestion (166, 179).”
BackgroundSham feeding corn oil increases accumbens dopamine in the rat
Liang, N.-C., Hajnal, A., & Norgren, R. (2006) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00226.2006 · Cited by 179
Localization of Leptin Receptor (Ob-R) Messenger Ribonucleic Acid in the Rodent Hindbrain
Mercer, J. G., Moar, K. M., & Hoggard, N. (1998) · Endocrinology · doi:10.1210/endo.139.1.5685 · Cited by 176
Symposium overview–food addiction: fact or fiction?
Corwin, R. L., & Grigson, P. S. (2009) · The Journal of Nutrition · doi:10.3945/jn.108.097691 · Cited by 175
Differential expression of mRNA for leptin receptor isoforms in the rat brain
Guan, X.-M., Hess, J. F., Yu, H., Hey, P. J., & van der Ploeg, L. H. T. (1997) · Molecular and Cellular Endocrinology · doi:10.1016/s0303-7207(97)00138-x · Cited by 173
Sugars: hedonic aspects, neuroregulation, and energy balance
Levine, A. S., Kotz, C. M., & Gosnell, B. A. (2003) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/78.4.834s · Cited by 170
Dugan, L. L., Ali, S. S., Shekhtman, G., Roberts, A. J., Lucero, J., Quick, K. L., & Behrens, M. M. (2009) · PLoS ONE · doi:10.1371/journal.pone.0005518 · Cited by 165
Rolls, E., Verhagen, J. V., & Kadohisa, M. (2003) · Journal of Neurophysiology · doi:10.1152/jn.00515.2003 · Cited by 164
Energy balance and weight regulation: genetics versus environment
Ravussin, E., & Bogardus, C. (2000) · British Journal of Nutrition · doi:10.1017/s0007114500000908 · Cited by 164
Leptin: a potential cognitive enhancer?
Harvey, J., Shanley, L. J., O'Malley, D., & Irving, A. J. (2005) · Biochemical Society Transactions · doi:10.1042/bst0331029 · Cited by 162
Effects of overfeeding on the neuronal response to visual food cues
Cornier, M.-A., Von Kaenel, S. S., Bessesen, D. H., & Tregellas, J. R. (2007) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/86.4.965 · Cited by 160
Localization of leptin receptor mRNA expression in mouse brain
Huang, X. F., Koutcherov, I., Lin, S., Wang, H. Q., & Storlien, L. (1996) · NeuroReport · doi:10.1097/00001756-199611040-00045 · Cited by 160
A Role for the Right Anterior Temporal Lobe in Taste Quality Recognition
Small, D. M., Jones‐Gotman, M., Zatorre, R. J., Petrides, M., & Evans, A. C. (1997) · Journal of Neuroscience · doi:10.1523/jneurosci.17-13-05136.1997 · Cited by 150
Consumption of a high-fat diet alters the homeostatic regulation of energy balance
Woods, S. C., D’Alessio, D. A., Tso, P., Rushing, P. A., Clegg, D. J., Benoit, S. C., Gotoh, K., Liu, M., & Seeley, R. J. (2004) · Physiology & Behavior · doi:10.1016/j.physbeh.2004.07.026 · Cited by 150
Balcita‐Pedicino, J. J., & Sesack, S. R. (2007) · Journal of Comparative Neurology · doi:10.1002/cne.21420 · Cited by 150
Brain Adipocytokine Action and Metabolic Regulation
Ahima, R. S., Qi, Y., Singhal, N. S., Jackson, M. B., & Scherer, P. E. (2006) · Diabetes · doi:10.2337/db06-s018 · Cited by 150
Individual differences in the neurophysiology of reward and the obesity epidemic
Small, D. M. (2009) · International Journal of Obesity · doi:10.1038/ijo.2009.71 · Cited by 144
Hypothalamic inflammation and energy homeostasis: Resolving the paradox
Thaler, J. P., Choi, S. J., Schwartz, M. W., & Wisse, B. E. (2010) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2009.10.002 · Cited by 144
Repeated sucrose access influences dopamine D2 receptor density in the striatum
Bello, N. T., Lucas, L. R., & Hajnal, A. (2002) · Neuroreport · doi:10.1097/00001756-200208270-00017 · Cited by 144
Role of dietary fat in calorie intake and weight gain
Warwick, Z. S., & Schiffman, S. S. (1992) · Neuroscience & Biobehavioral Reviews · doi:10.1016/s0149-7634(05)80198-8 · Cited by 141
Hoebel, B. G. (1969) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1969.tb12919.x · Cited by 138
Brain Pathways Controlling Food Intake and Body Weight
Schwartz, M. W. (2001) · Experimental Biology and Medicine · doi:10.1177/153537020122601103 · Cited by 135
Bingeing rats: A model of intermittent excessive behavior?
Corwin, R. L. (2006) · Appetite · doi:10.1016/j.appet.2004.09.002 · Cited by 134
The nucleus accumbens and reward: neurophysiological investigations in behaving animals
Carelli, R. M. (2002) · Behavioral and Cognitive Neuroscience Reviews · doi:10.1177/1534582302238338 · Cited by 131
Combined dieting and stress evoke exaggerated responses to opioids in binge-eating rats.
Boggiano, M. M., Chandler, P. C., Viana, J. B., Oswald, K. D., Maldonado, C. R., & Wauford, P. K. (2005) · Behavioral Neuroscience · doi:10.1037/0735-7044.119.5.1207 · Cited by 131
Grigson, P. S. (2002) · Physiology & Behavior · doi:10.1016/s0031-9384(02)00758-8 · Cited by 130
Teegarden, S. L., Scott, A., & Bale, T. L. (2009) · Neuroscience · doi:10.1016/j.neuroscience.2009.05.029 · Cited by 123
Davidowa, H., Li, Y., & Plagemann, A. (2003) · European Journal of Neuroscience · doi:10.1046/j.1460-9568.2003.02789.x · Cited by 123
Keen‐Rhinehart, E., & Bartness, T. J. (2004) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00705.2004 · Cited by 120
Carlini, V., Martini, A., Schiöth, H., Ruiz, R., de Cuneo, M. F., & Debarioglio, S. R. (2008) · Neuroscience · doi:10.1016/j.neuroscience.2008.03.015 · Cited by 119
Fasting Activates the Nonhuman Primate Hypocretin (Orexin) System and Its Postsynaptic Targets
Diano, S., Horvath, B., Urbanski, H. F., Sotonyi, P., & Horvath, T. L. (2003) · Endocrinology · doi:10.1210/en.2003-0274 · Cited by 119
JULLIARD, A., CHAPUT, M., APELBAUM, A., AIME, P., MAHFOUZ, M., & DUCHAMPVIRET, P. (2007) · Behavioural Brain Research · doi:10.1016/j.bbr.2007.05.033 · Cited by 119
Direct Innervation and Modulation of Orexin Neurons by Lateral Hypothalamic LepRb Neurons
Louis, G. W., Leinninger, G. M., Rhodes, C. J., & Myers, M. G. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.1340-10.2010 · Cited by 113
The hypocretins as sensors for metabolism and arousal
Adamantidis, A., & De Lecea, L. (2009) · The Journal of Physiology · doi:10.1113/jphysiol.2008.164400 · Cited by 112
Bello, N. T., Sweigart, K. L., Lakoski, J. M., Norgren, R., & Hajnal, A. (2003) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00716.2002 · Cited by 112
Modulation of the mesolimbic dopamine system by leptin
Opland, D. M., Leinninger, G. M., & Myers (2010) · Brain Research · doi:10.1016/j.brainres.2010.04.028 · Cited by 111
The neurocognitive bases of human multimodal food perception: Consciousness
Verhagen, J. V. (2006) · Brain Research Reviews · doi:10.1016/j.brainresrev.2006.09.002 · Cited by 110
Shin, A. C., Pistell, P. J., Phifer, C. B., & Berthoud, H. R. (2010) · Neuroscience · doi:10.1016/j.neuroscience.2010.07.017 · Cited by 109
Self-citationVariety in the flavor of food enhances eating in the rat: A controlled demonstration☆
Treit, D., Spetch, M. L., & Deutsch, J. A. (1983) · Physiology & Behavior · doi:10.1016/0031-9384(83)90007-0 · Cited by 106
Time-dependent changes in alcohol-seeking behaviour during abstinence
Bieńkowski, P. (2004) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2003.10.005 · Cited by 103
Carbohydrate-induced hyperphagia and obesity in the rat: Effects of saccharide type, form, and taste
Sclafani, A. (1987) · Neuroscience & Biobehavioral Reviews · doi:10.1016/s0149-7634(87)80020-9 · Cited by 100
Leptin regulates olfactory-mediated behavior in ob/ob mice
Getchell, T. V., Kwong, K., Saunders, C. P., Stromberg, A. J., & Getchell, M. L. (2006) · Physiology & Behavior · doi:10.1016/j.physbeh.2005.11.016 · Cited by 96
Presynaptic NMDA receptor subunit immunoreactivity in GABAergic terminals in rat brain
Paquet, M., & Smith, Y. (2000) · The Journal of Comparative Neurology · doi:10.1002/1096-9861(20000724)423:2 · Cited by 95
Hoebel, B. G. (1968) · Journal of Comparative and Physiological Psychology · doi:10.1037/h0025962 · Cited by 92
Accumbens dopamine mediates the rewarding effect of orosensory stimulation by sucrose
Smith, G. P. (2004) · Appetite · doi:10.1016/j.appet.2004.02.006 · Cited by 87
Environmental enrichment attenuates cue-induced reinstatement of sucrose seeking in rats
Grimm, J. W., Osincup, D., Wells, B., Manaois, M., Fyall, A., Buse, C., & Harkness, J. H. (2008) · Behavioural Pharmacology · doi:10.1097/fbp.0b013e32831c3b18 · Cited by 85
Genetically Determined Differences in Brain Response to a Primary Food Reward: Figure 1.
Felsted, J. A., Ren, X., Chouinard-Decorte, F., & Small, D. M. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.5483-09.2010 · Cited by 84
Intermittent access to preferred food reduces the reinforcing efficacy of chow in rats
Cottone, P., Sabino, V., Steardo, L., & Zorrilla, E. P. (2008) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.90309.2008 · Cited by 84
The Neurophysiology of Taste and Olfaction in Primates, and Umami Flavora
ROLLS, E. T., CRITCHLEY, H. D., BROWNING, A., & HERNADI, I. (1998) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1998.tb10602.x · Cited by 80
The relationship between food reward and satiation revisited
Sclafani, A., & Ackroff, K. (2004) · Physiology & Behavior · doi:10.1016/j.physbeh.2004.04.045 · Cited by 80
Regulation of adaptive behaviour during fasting by hypothalamic Foxa2
Silva, J., von Meyenn, F., Howell, J. J., Thorens, B., Wolfrum, C., & Stoffel, M. (2009) · Nature · doi:10.1038/nature08589 · Cited by 79
Obesity exacerbates chemically induced neurodegeneration
Sriram, K., Benkovic, S. A., Miller, D. B., & O’Callaghan, J. P. (2002) · Neuroscience · doi:10.1016/s0306-4522(02)00306-8 · Cited by 78
Neural correlates of individual differences related to appetite
Lowe, M. R., van Steenburgh, J., Ochner, C. N., & Coletta, M. C. (2009) · Physiology & Behavior · doi:10.1016/j.physbeh.2009.04.001 · Cited by 70
Obesity by choice: the powerful influence of nutrient availability on nutrient intake
Tordoff, M. G. (2002) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00739.2001 · Cited by 69
Orexin-A Hyperphagia: Hindbrain Participation in Consummatory Feeding Responses
Baird, J.-P., Choe, A., Loveland, J. L., Beck, J., Mahoney, C. E., Lord, J. S., & Grigg, L. A. (2009) · Endocrinology · doi:10.1210/en.2008-0293 · Cited by 65
Velkoska, E., Cole, T. J., Dean, R. G., Burrell, L. M., & Morris, M. J. (2008) · Journal of Nutrition · doi:10.1093/jn/138.9.1622 · Cited by 64
Parigi, A. D., Chen, K., Salbe, A. D., Reiman, E. M., & Tataranni, P. A. (2003) · Obesity Research · doi:10.1038/oby.2003.68 · Cited by 61
Naloxone attenuates incubated sucrose craving in rats
Grimm, J. W., Manaois, M., Osincup, D., Wells, B., & Buse, C. (2007) · Psychopharmacology · doi:10.1007/s00213-007-0868-y · Cited by 56
LRb signals act within a distributed network of leptin‐responsive neurones to mediate leptin action
Leinninger, G. M., & Myers, M. G. (2008) · Acta Physiologica · doi:10.1111/j.1748-1716.2007.01784.x · Cited by 56
BLUNDELL, J. E., & HERBERG, L. J. (1968) · Nature · doi:10.1038/219627a0 · Cited by 53
Kaczmarek, H. J., & Kiefer, S. W. (2000) · Pharmacology Biochemistry and Behavior · doi:10.1016/s0091-3057(00)00182-9 · Cited by 52
Sucrose Exposure in Early Life Alters Adult Motivation and Weight Gain
Frazier, C. R. M., Mason, P., Zhuang, X., & Beeler, J. A. (2008) · PLoS ONE · doi:10.1371/journal.pone.0003221 · Cited by 52
Functional Role of c-Jun-N-Terminal Kinase in Feeding Regulation
Unger, E. K., Piper, M. L., Olofsson, L. E., & Xu, A. W. (2009) · Endocrinology · doi:10.1210/en.2009-0711 · Cited by 50
Editors' Introduction: Issues in Adolescent Substance Abuse Treatment
Jainchill, N., & Margolis, R. D. (2000) · Journal of Psychoactive Drugs · doi:10.1080/02791072.2000.10400206 · Cited by 48
Research works printed but not linked: 2
- Rosenbaum M, 2008, J Clin Invest, 118, 2583
- Verhagen JV, 2006, Brain Res Brain Res Rev
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Asarian, L., & Geary, N. (2013) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00446.2012 · Cited by 513
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Self-citation
Metadata
- Authors
- Berthoud, H.-R., Lenard, N. R., & Shin, A. C.
- Affiliations
- Pennington Biomedical Research Center (US)
- Corresponding author
- Berthoud, Hans-Rudolf
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2011-06
- Volume
- 300
- Issue
- 6
- Pages
- R1266-R1277
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC3119156
- OpenAlex
- W2141794225
- Cited by
- 275
- References
- 208
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 4 · 2023: 16 · 2022: 10 · 2021: 24 · 2020: 18 · 2019: 52 · 2018: 11 · 2017: 12 · 2016: 17 · 2015: 20 · 2014: 27 · 2013: 25 · 2012: 18
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-47348, R01DK071082, DK071082, R01DK047348)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
- Keywords
- food reward, hyperphagia, obesity, incentive salience, palatable food intake, brain reward system, sensitization, inflammatory signaling, oxidative stress, mitochondrial stress, drug addiction, alcoholism, eating disorders, obesity-related comorbidities
- MeSH terms
- Animals, Humans, Hyperphagia, Neural Pathways, Obesity, Reward, Signal Transduction, Behavior, Addictive, Models, Animal
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