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
Research works printed but not linked: 2
- Rosenbaum M, 2008, J Clin Invest, 118, 2583
- Verhagen JV, 2006, Brain Res Brain Res Rev
Cited by
Sorted by citations
Neurobiology of food intake in health and disease
Morton, G. J., Meek, T. H., & Schwartz, M. W. (2014) · Nature Reviews Neuroscience · doi:10.1038/nrn3745 · Cited by 748
Sex differences in the physiology of eating
Asarian, L., & Geary, N. (2013) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00446.2012 · Cited by 513
“Liking” and “wanting” in eating and food reward: Brain mechanisms and clinical implications
Morales, I., & Berridge, K. C. (2020) · Physiology & Behavior · doi:10.1016/j.physbeh.2020.113152 · Cited by 346
Singh, M. (2014) · Frontiers in Psychology · doi:10.3389/fpsyg.2014.00925 · Cited by 337
The neurobiology of food intake in an obesogenic environment
Berthoud, H. (2012) · Proceedings of The Nutrition Society · doi:10.1017/s0029665112000602 · Cited by 319
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
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