Central nervous system control of food intake

Schwartz, Michael W.; Woods, Stephen C.; Porte, Daniel; Seeley, Randy J.; Baskin, Denis G.

doi:10.1038/35007534

Cited by 6,451Regulation of Appetite and ObesityHypothalamic control of reproductive hormonesAdipokines, Inflammation, and Metabolic Diseases

Central nervous system control of food intake

Schwartz, Michael W., Woods, Stephen C., Porte, Daniel, Seeley, Randy J., Baskin, Denis G.·2000·Nature

DOI 10.1038/35007534

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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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Individual populations of neurons within a given hypothalamic nucleus may have opposing effects, as with POMC and AGRP neurons in the arcuate nucleus.
“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]
Insulin has important central nervous system effects, where its action in the hypothalamus reduces food intake and increases energy expenditure.
“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]
The arcuate nucleus contains orexigenic NPY/AGRP/GABA neurons and anorexigenic alpha-MSH/CART neurons.
“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]
Two antagonistic neuronal populations in the arcuate nucleus, orexigenic NPY/AGRP/GABA neurons and anorexigenic α-MSH/CART neurons, are primarily responsible for sensing and relaying information to hypophysiotropic TRH neurons about blood leptin concentration.
“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]
Fasting lowers leptin, which stimulates NPY/AGRP neurons and suppresses α-MSH/CART neurons.
“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 lean healthy individuals, peripheral and central insulin infusion suppresses appetite and feeding.
“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
Leptin is crucial to integrate the melanocortin neuronal circuit of the hypothalamus with the energy stores of the body.
“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]
Norepinephrine, dopamine, and serotonin are important in central energy balance.
“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]
POMC neurons are depolarized by leptin, leading to release of α-MSH, which mediates anorexigenic effects through activation of melanocortin receptors.
“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
Meal-related humoral signals can be modulated by long-term homeostatic signals influenced by body energy stores, namely leptin, insulin, and ghrelin.
“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]
Leptin is a hormone produced mainly by adipocytes and is implicated in a wide variety of physiological functions, especially regulation of energy balance.
“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]
Leptin is secreted in increasing amounts as adipocytes enlarge.
“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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Leptin actions on food intake and body temperature are mediated by IL-1
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Expression of Leptin Receptor Isoforms in Rat Brain Microvessels
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Ascending projections from the solitary tract nucleus to the hypothalamus. A Phaseolus vulgaris lectin tracing study in the rat
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Distribution and phenotype of neurons containing the ATP-sensitive K+ channel in rat brain
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Restricted eating with weight loss selectively decreases extracellular dopamine in the nucleus accumbens and alters dopamine response to amphetamine, morphine, and food intake
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Central leptin modulates behavioral and neural responsivity to CCK
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Physiological and Anatomical Circuitry between Agouti-Related Protein and Leptin Signaling
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Leptin increases serotonin turnover by inhibition of brain nitric oxide synthesis
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Evidence That Plasma Leptin and Insulin Levels are Associated With Body Adiposity Via Different Mechanisms
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Tyrosine Phosphorylation of Tub and Its Association with Src Homology 2 Domain-containing Proteins Implicate Tub in Intracellular Signaling by Insulin
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Energy balance in man studies carried out by the Division of Human Physiology, National Institute for Medical Research.
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The arcuate nucleus is pivotal in mediating the anorectic effects of centrally administered leptin
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Mechanisms linking obesity to insulin resistance and type 2 diabetes
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Ghrelin enhances appetite and increases food intake in humans
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Biological, Physiological, Pathophysiological, and Pharmacological Aspects of Ghrelin
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Metabolism disrupting chemicals and metabolic disorders
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The Need to Feed
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Mechanisms of leptin action and leptin resistance.
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The vagus nerve and the inflammatory reflex – linking immunity and metabolism
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STAT3 signalling is required for leptin regulation of energy balance but not reproduction
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Gut Hormone Profiles Following Bariatric Surgery Favor an Anorectic State, Facilitate Weight Loss, and Improve Metabolic Parameters
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Authors: Schwartz, M. W., Woods, S. C., Porte, D., Seeley, R. J., & Baskin, D. G.
Affiliations: University of Washington (US)
University of Cincinnati (US)
ORCID: Schwartz, Michael W.
Woods, Stephen C.
Seeley, Randy J.
Baskin, Denis G.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2000-04
Volume: 404
Issue: 6778
Pages: 661-671
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/35007534
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 › Epidemiology › 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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Central nervous system control of food intake

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