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Sixteen years and counting: an update on leptin in energy balance
Open accessAbstract
Cloned in 1994, the ob gene encodes the protein hormone leptin, which is produced and secreted by white adipose tissue. Since its discovery, leptin has been found to have profound effects on behavior, metabolic rate, endocrine axes, and glucose fluxes. Leptin deficiency in mice and humans causes morbid obesity, diabetes, and various neuroendocrine anomalies, and replacement leads to decreased food intake, normalized glucose homeostasis, and increased energy expenditure. Here, we provide an update on the most current understanding of leptin-sensitive neural pathways in terms of both anatomical organization and physiological roles.
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“Leptin is satiety promoting hormone produced and secreted primarily by adipose tissue that helps to regulate energy balance by reducing food intake and increasing energy expenditure via activation of hypothalamic circuits.56,57”
From The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review (2024) · cites this paper as [57]
In the citing paper
“Circulating leptin changes rapidly in response to acute caloric intake or restriction, assisting in the control of short-term feeding via mechanisms such as augmentation of the anorectic effects of cholecystokinin, [57][58][59]”
From The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review (2024) · cites this paper as [57]
In the citing paper
“and is thought to be an important mediator of long-term energy balance regulation.57”
From The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review (2024) · cites this paper as [57]
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Metadata
- Authors
- Gautron, L., & Elmquist, J. K.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Elmquist, Joel K.
- ORCID
- Elmquist, Joel K.
- Venue
- Journal of Clinical Investigation
- Published
- 2011-06-01
- Volume
- 121
- Issue
- 6
- Pages
- 2087-2093
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3104762
- OpenAlex
- W2068769790
- Cited by
- 367
- References
- 128
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 4 · 2023: 11 · 2022: 8 · 2021: 10 · 2020: 18 · 2019: 17 · 2018: 17 · 2017: 26 · 2016: 28 · 2015: 33 · 2014: 52 · 2013: 52 · 2012: 66
- FWCI
- 5.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Michigan
- 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
- leptin, ob gene, energy balance, white adipose tissue, leptin deficiency, morbid obesity, diabetes mellitus, glucose homeostasis, dietary intake, energy expenditure, neuroendocrine regulation, metabolic rate
- MeSH terms
- Adaptation, Physiological, Animals, Body Weight, Brain, Disease Models, Animal, Energy Metabolism, Feeding Behavior, Glucose, Humans, Hypothalamus, Mice, Obese, Models, Biological, Pro-Opiomelanocortin, Starvation, Sympathetic Nervous System, Leptin, Receptor, Melanocortin, Type 4, Overnutrition, Mice, Adipose Tissue, White, Receptors, Leptin
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