Unraveling the central nervous system pathways underlying responses to leptin
Abstract
Here we summarize recent progress in the biology of leptin, concentrating on its central nervous system (CNS) actions. The product of the ob gene, leptin is a circulating hormone produced by white adipose tissue that has potent effects on feeding behavior, thermogenesis and neuroendocrine responses. Leptin regulates energy homeostasis, as its absence in rodents and humans causes severe obesity. We consider the physiological mechanisms underlying leptin action, along with several novel hypothalamic neuropeptides that affect food intake and body weight. The molecular causes of several other obesity syndromes are discussed to illuminate how the CNS regulates body weight. We describe neural circuits that are downstream of leptin receptors and propose a model linking populations of leptin-responsive neurons with effector neurons underlying leptin's endocrine, autonomic and behavioral effects.
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To date there is limited evidence that leptin mediates thermogenesis via the SNS in humans.
“In addition, leptin, released by white adipocytes, regulates energy balance by effects on the hypothalamus that lead to inhibition of food intake and increased thermogenesis via activation of the SNS, though to date there is limited evidence that leptin mediates thermogenesis via the SNS in humans 66–70.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [68]
Leptin, released by white adipocytes, regulates energy balance by effects on the hypothalamus that lead to inhibition of food intake and increased thermogenesis via activation of the SNS.
“In addition, leptin, released by white adipocytes, regulates energy balance by effects on the hypothalamus that lead to inhibition of food intake and increased thermogenesis via activation of the SNS, though to date there is limited evidence that leptin mediates thermogenesis via the SNS in humans 66–70.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [68]
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References 105 · Cited by 520
- Authors
- Elmquist, J. K., Maratos-Flier, E., Saper, C. B., & Flier, J. S.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Elmquist, Joel K.
- Venue
- Nature Neuroscience
- Published
- 1998-10
- Volume
- 1
- Issue
- 6
- Pages
- 445-450
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- DOI
- 10.1038/2164
- OpenAlex
- W1594976448
- Cited by
- 520
- References
- 105
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 3 · 2023: 6 · 2022: 4 · 2021: 7 · 2020: 10 · 2019: 11 · 2018: 12 · 2017: 15 · 2016: 12 · 2015: 13 · 2014: 23 · 2013: 19 · 2012: 21
- FWCI
- 3.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- leptin, central nervous system, hypothalamus, feeding behavior, energy homeostasis, obesity, leptin receptor, hypothalamic neuropeptides, thermogenesis, neuroendocrine regulation, neural circuits, body weight regulation, autonomic effects
- MeSH terms
- Brain, Humans, Hypothalamic Area, Lateral, Models, Neurological, Obesity, Proteins, Starvation, Leptin
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