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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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
“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]
Citations
Cites
Positional cloning of the mouse obese gene and its human homologue
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994) · Nature · doi:10.1038/372425a0 · Cited by 13,419
Serum Immunoreactive-Leptin Concentrations in Normal-Weight and Obese Humans
Considine, R. V., Sinha, M. K., Heiman, M. L., Kriauciunas, A., Stephens, T. W., Nyce, M. R., Ohannesian, J. P., Marco, C. C., McKee, L. J., Bauer, T. L., et al. (1996) · New England Journal of Medicine · doi:10.1056/nejm199602013340503 · Cited by 6,326
Sakurai, T., Amemiya, A., Ishii, M., Matsuzaki, I., Chemelli, R. M., Tanaka, H., Williams, S. C., Richardson, J. A., Kozlowski, G. P., Wilson, S., et al. (1998) · Cell · doi:10.1016/s0092-8674(00)80949-6 · Cited by 5,501
The hypocretins: hypothalamus-specific peptides with neuroexcitatory activity
de Lecea, L., Kilduff, T. S., Peyron, C., Gao, X.-B., Foye, P. E., Danielson, P. E., Fukuhara, C., Battenberg, E. L. F., Gautvik, V. T., Bartlett, F. S., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.1.322 · Cited by 3,878
Identification and expression cloning of a leptin receptor, OB-R.
Tartaglia, L. A., Dembski, M., Weng, X., Deng, N., Culpepper, J., Devos, R., Richards, G. J., Campfield, L. A., Clark, F. T., Deeds, J., et al. (1995) · Cell · doi:10.1016/0092-8674(95)90151-5 · Cited by 3,496
Campfield, L. A., Smith, F. J., Guisez, Y., Devos, R., & Burn, P. (1995) · Science · doi:10.1126/science.7624778 · Cited by 3,243
Narcolepsy in orexin Knockout Mice
Chemelli, R. M., Willie, J. T., Sinton, C. M., Elmquist, J. K., Scammell, T., Lee, C., Richardson, J. A., Williams, S. C., Xiong, Y., Kisanuki, Y., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)81973-x · Cited by 3,095
Targeted disruption of the melanocortin-4 receptor results in obesity in mice
Huszar, D., Lynch, C. A., Fairchild-Huntress, V., Dunmore, J. H., Fang, Q., Berkemeier, L. R., Gu, W., Kesterson, R. A., Boston, B. A., Cone, R. D., et al. (1997) · Cell · doi:10.1016/s0092-8674(00)81865-6 · Cited by 3,030
Congenital leptin deficiency is associated with severe early-onset obesity in humans
Montague, C. T., Farooqi, I. S., Whitehead, J. P., Soos, M. A., Rau, H., Wareham, N. J., Sewter, C. P., Digby, J. E., Mohammed, S. N., Hurst, J. A., et al. (1997) · Nature · doi:10.1038/43185 · Cited by 2,936
A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction
Clément, K., Vaisse, C., Lahlou, N., Cabrol, S., Pelloux, V., Cassuto, D., Gourmelen, M., Dina, C., Chambaz, J., Lacorte, J.-M., et al. (1998) · Nature · doi:10.1038/32911 · Cited by 2,346
Research works printed but not linked: 3
- Edholm, O. G. Energy balance in man. J. Human Nutr. 31, 413–431 (1977).
- Bray, G. A., Fisler, J. & York, D. A. Neuroendocrine control of the development of obesity: understanding gained from studies of experimental animal models. Front. Neuroendocrinol. 11, 128–181 (1990).
- Hagan, M. et al. Effect of agouti-related peptide (83-132) on food intake: competitive melanocortin-receptor antagonism on short but not long term effects. Am. J. Physiol. (in the press).
Cited by
Sorted by citations
Mechanisms linking obesity to insulin resistance and type 2 diabetes
Kahn, S. E., Hull, R. L., & Utzschneider, K. M. (2006) · Nature · doi:10.1038/nature05482 · Cited by 5,448
DeFronzo, R. A. (2009) · Diabetes · doi:10.2337/db09-9028 · Cited by 3,016
Ghrelin: Structure and Function
Kojima, M., & Kangawa, K. (2005) · Physiological Reviews · doi:10.1152/physrev.00012.2004 · Cited by 2,810
Central nervous system control of food intake and body weight
Morton, G. J., Cummings, D. E., Baskin, D. G., Barsh, G. S., & Schwartz, M. W. (2006) · Nature · doi:10.1038/nature05026 · Cited by 2,503
Self-citationTaheri, S., Lin, L., Austin, D., Young, T., & Mignot, E. (2004) · PLoS Medicine · doi:10.1371/journal.pmed.0010062 · Cited by 2,477
“Leptin administration suppresses food intake and reduces energy expenditure [21,22].”
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
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
