The DOI matches its Crossref record; 123 of the 123 references it cites were found in a registry or an index.
Central nervous system control of food intake
Abstract
New information regarding neuronal circuits that control food intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its importance to human health. Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity, the growing number of such signalling molecules indicates that food intake is controlled by a highly complex process. To better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.
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In the citing paper
“Individual populations of neurons within a given hypothalamic nucleus may have opposing effects, as with POMC and AGRP neurons in the arcuate nucleus52.”
From IDOL regulates systemic energy balance through control of neuronal VLDLR expression (2019) · cites this paper as [52]
In the citing paper
“In addition to its critical role in regulating glucose, lipid and protein metabolism, insulin also has important central nervous system effects, where its action in the hypothalamus reduces food intake and increases energy expenditure [155].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [155]
In the citing paper
“Two major feeding-related neuronal populations are involved: the medially located, orexigenic neurons that synthesize neuropeptide Y (NPY), AGRP, and ␥-amino butyric acid (GABA); and laterally located anorexigenic neurons that produce ␣-MSH and CART (56).”
From Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions (2014) · cites this paper as [56]
In the citing paper
“Two antagonistic, neuronal populations in the arcuate nucleus, the orexigenic NPY/AGRP/GABA neurons and the anorexigenic ␣-MSH/CART neurons, are primarily responsible for sensing and relaying information to hypophysiotropic TRH neurons about the concentration of leptin in the bloodstream (56)”
From Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions (2014) · cites this paper as [56]
In the citing paper
“Because the fasting-induced fall of leptin stimulates NPY/AGRP neurons and inhibits ␣-MSH/CART neurons (56)”
From Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions (2014) · cites this paper as [56]
In the citing paper
“in lean healthy individuals, peripheral and even central infusion of insulin suppresses appetite and feeding”
From Role of addiction and stress neurobiology on food intake and obesity (2018) · cites this paper as Schwartz, Woods, Porte, Seeley, & Baskin, 2000
In the citing paper
“The adipose tissue-derived hormone, leptin, is crucial to integrate the melanocortin neuronal circuit of the hypothalamus with the energy stores of the body [34-36].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [36]
In the citing paper
“The neurotransmitters norepinephrine, dopamine and serotonin are also important in central energy balance [34, 36]”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [36]
In the citing paper
“POMC neurons are depolarized by leptin, leading to release of α-melanocyte stimulating hormone (α-MSH), a POMC-derived neuropeptide that mediates its anorexigenic effects through activation of melanocortin receptors (Cone, 2005; Cowley et al., 2001; Schwartz et al., 2000).”
From Leptin-Dependent Control of Glucose Balance and Locomotor Activity by POMC Neurons (2009) · cites this paper as Schwartz et al., 2000
In the citing paper
“In addition, these meal-related humeral signals can be modulated by the more tonic, or long-term, homeostatic signals which are influenced by body energy stores, namely leptin, insulin [11,12], and ghrelin [13].”
From Homeostatic and Circadian Control of Food Intake: Clinical Strategies to Prevent Overconsumption (2013) · cites this paper as [12]
In the citing paper
“Leptin is a hormone that is produced mainly by adipocytes and has been implicated in a wide variety of physiological functions, especially in the regulation of energy balance119,120.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [120]
In the citing paper
“In contrast to adiponectin, leptin is secreted in increasing amounts as adipocytes enlarge119,120.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [120]
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Hypothalamic sensing of fatty acids
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Modulation of Blood Pressure by Central Melanocortinergic Pathways
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Evidence That the Caudal Brainstem Is a Target for the Inhibitory Effect of Leptin on Food Intake
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Metadata
- Authors
- Schwartz, M. W., Woods, S. C., Porte, D., Seeley, R. J., & Baskin, D. G.
- Affiliations
- University of Washington (US)
- University of Cincinnati (US)
- Venue
- Nature
- Published
- 2000-04
- Volume
- 404
- Issue
- 6778
- Pages
- 661-671
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1561443084
- Cited by
- 6,451
- References
- 123
- Citations by year
- 2026: 87 · 2025: 126 · 2024: 138 · 2023: 123 · 2022: 153 · 2021: 210 · 2020: 184 · 2019: 206 · 2018: 223 · 2017: 255 · 2016: 292 · 2015: 316 · 2014: 305 · 2013: 367 · 2012: 339
- FWCI
- 22.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- food intake regulation, energy homeostasis, hypothalamus, neuropeptides, hormone signaling, obesity, neural circuits, energy expenditure
- MeSH terms
- Central Nervous System, Eating, Energy Metabolism, Homeostasis, Humans, Hypothalamus, Insulin, Models, Biological, Neuropeptides, Obesity, Satiation, Biogenic Monoamines, Signal Transduction, Leptin
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