The DOI matches its Crossref record; 292 of the 293 references it cites were found in a registry or an index.
Brain regulation of energy balance and body weight
Open accessAbstract
Body weight is determined by a balance between food intake and energy expenditure. Multiple neural circuits in the brain have evolved to process information about food, food-related cues and food consumption to control feeding behavior. Numerous gastrointestinal endocrine cells produce and secrete satiety hormones in response to food consumption and digestion. These hormones suppress hunger and promote satiation and satiety mainly through hindbrain circuits, thus governing meal-by-meal eating behavior. In contrast, the hypothalamus integrates adiposity signals to regulate long-term energy balance and body weight. Distinct hypothalamic areas and various orexigenic and anorexigenic neurons have been identified to homeostatically regulate food intake. The hypothalamic circuits regulate food intake in part by modulating the sensitivity of the hindbrain to short-term satiety hormones. The hedonic and incentive properties of foods and food-related cues are processed by the corticolimbic reward circuits. The mesolimbic dopamine system encodes subjective "liking" and "wanting" of palatable foods, which is subjected to modulation by the hindbrain and the hypothalamic homeostatic circuits and by satiety and adiposity hormones. Satiety and adiposity hormones also promote energy expenditure by stimulating brown adipose tissue (BAT) activity. They stimulate BAT thermogenesis mainly by increasing the sympathetic outflow to BAT. Many defects in satiety and/or adiposity hormone signaling and in the hindbrain and the hypothalamic circuits have been described and are believed to contribute to the pathogenesis of energy imbalance and obesity.
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In the citing paper
“Nutrient supplementation with fiber, resistant starch, and unsaturated fats are the most studied supplements in both animal studies and small‐scale human trials—often showing increased circulating GLP‐1 concentrations and associated metabolic improvements [269].”
From Nutritional priorities to support GLP ‐1 therapy for obesity: A joint Advisory from the American College of Lifestyle Medicine, the American Society for Nutrition, the Obesity Medicine Association, and The Obesity Society (2025) · cites this paper as [269]
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“Nutrient supplementation with fiber, resistant starch, and unsaturated fats are the most studied supplements in both animal studies and small-scale human trials—often showing increased circulating GLP-1 concentrations and associated metabolic improvements [269].”
In the citing paper
“Insulin and leptin are the main anorexigenic hormones and inform the hypothalamus, particularly the arcuate nucleus of the hypothalamus (ARC), the master regulator of energy balance, about longand short-term energy status.[143,144]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [143]
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Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus
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Role of Brain Insulin Receptor in Control of Body Weight and Reproduction
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Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein
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Volkoff, H. (2016) · Frontiers in Neuroscience · doi:10.3389/fnins.2016.00540 · Cited by 357
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Murray, S. M., Tulloch, A. J., Gold, M. S., & Avena, N. M. (2014) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2014.91 · Cited by 275
Anti-obesogenic and antidiabetic effects of plants and mushrooms
Martel, J., Ojcius, D. M., Chang, C., Lin, C.-S., Lu, C., Ko, Y., Tseng, S., Lai, H., & Young, J. D. (2016) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.142 · Cited by 270
The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction
Sergi, D., Boulestin, H., Campbell, F. M., & Williams, L. M. (2021) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201900934 · Cited by 194
Brown and Beige Adipose Tissues in Health and Disease
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Self-citation
Metadata
- Authors
- Rui, L.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Rui, Liangyou
- ORCID
- Rui, Liangyou
- Venue
- Reviews in Endocrine and Metabolic Disorders
- Published
- 2013-08-30
- Volume
- 14
- Issue
- 4
- Pages
- 387-407
- ISSN
- 1389-9155 (ISSN-L)
- 1573-2606
- PMC
- PMC3817823
- OpenAlex
- W2090476959
- Cited by
- 168
- References
- 293
- Citations by year
- 2026: 8 · 2025: 17 · 2024: 10 · 2023: 7 · 2022: 15 · 2021: 12 · 2020: 14 · 2019: 10 · 2018: 24 · 2017: 18 · 2016: 13 · 2015: 12 · 2014: 7 · 2013: 1
- FWCI
- 1.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Reviews in Endocrine and Metabolic Disorders (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r01dk094014-04)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK091591, R01 DK-094014, R01DK065122, P30DK020572)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- energy balance, body weight regulation, feeding behavior, satiety hormones, hypothalamus, adiposity signals, mesolimbic dopamine system, brown adipose tissue thermogenesis, sympathetic outflow, obesity pathogenesis, energy imbalance
- MeSH terms
- Appetite Regulation, Body Weight, Brain, Energy Metabolism, Homeostasis, Humans, Nerve Net, Satiety Response
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