Leptin and the maintenance of elevated body weight
Abstract
Obesity represents the single most important risk factor for early disability and death in developed societies, and the incidence of obesity remains at staggering levels. CNS systems that modulate energy intake and expenditure in response to changes in body energy stores serve to maintain constant body adiposity; the adipocyte-derived hormone leptin and its receptor (LEPR) represent crucial regulators of these systems. As in the case of insulin resistance, a variety of mechanisms (including feedback inhibition, inflammation, gliosis and endoplasmic reticulum stress) have been proposed to interfere with leptin action and impede the systems that control body energy homeostasis to promote or maintain obesity, although the relative importance and contribution of each of these remain unclear. However, LEPR signalling may be increased (rather than impaired) in common obesity, suggesting that any obesity-associated defects in leptin action must result from lesions somewhere other than the initial LEPR signal. It is also possible that increased LEPR signalling could mediate some of the obesity-associated changes in hypothalamic function.
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Leptin enhances SNS outflow to induce thermogenesis.
“It also enhances SNS outflow to induce thermogenesis [225].”
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 [119]
In the central nervous system, leptin increases Janus tyrosine kinase 2 activity and activates three primary intracellular pathways: STAT3, SHP2-MAPK, and IRS2-PI3K signalling.
“In the CNS, leptin increases Janus tyrosine kinase 2 (JAK2) activity and activates three primary intracellular pathways: phosphorylation of LepR at Tyrl 138 recruits latent signal transducer and activator of transcription 3 (STAT3); phosphorylation of LepR at Tyr985 recruits Src homology 2 tyrosine phosphatase (SHP2) to activate mitogen-activated protein kinase (MAPK); and autophosphorylation of J”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [119]
The leptin receptor is expressed in multiple regions of the forebrain and hindbrain, including the hypothalamus, brainstem vasomotor centres, and intermediolateral nucleus of the spinal cord.
“The LepR is expressed in multiple regions of the forebrain and hindbrain, including the hypothalamus, brainstem vasomotor centres and intermediolateral nucleus (IML) of the spinal cord119,135,138 (FIG. 5a).”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [119]
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 [119]
Animals sense and adaptively respond to the restriction of energy, and this adaptive response is mediated principally by endocrine hormones that act directly in the brain as signals of energy status.
“it is now well accepted that animals sense and adaptively respond to the restriction of energy, and that this adaptive response is mediated principally by endocrine hormones that act directly in the brain as signals of energy status.”
From FGF21 and the physiological regulation of macronutrient preference (2020) · cites this paper as [23]
Leptin suppresses food intake and production of adrenal corticosteroids while promoting energy expenditure and decreasing insulin secretion.
“Indeed, leptin suppresses food intake and the production of adrenal corticosteroids while promoting energy expenditure and decreasing insulin secretion 38, 39.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [38]
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Self-citation
- Authors
- Pan, W. W., & Myers, M. G.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Myers, Martin G.
- Venue
- Nature reviews. Neuroscience
- Published
- 2018-01-11
- Volume
- 19
- Issue
- 2
- Pages
- 95-105
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- OpenAlex
- W2782974118
- Cited by
- 344
- References
- 101
- Citations by year
- 2026: 20 · 2025: 30 · 2024: 34 · 2023: 37 · 2022: 40 · 2021: 56 · 2020: 64 · 2019: 42 · 2018: 21
- FWCI
- 6.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (T32GM007315)
- 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, leptin receptor, obesity, leptin resistance, energy homeostasis, food intake regulation, hypothalamic function, inflammation, gliosis, endoplasmic reticulum stress, leptin signaling, weight maintenance
- MeSH terms
- Animals, Body Weight, Energy Metabolism, Homeostasis, Humans, Obesity, Signal Transduction, Leptin, Receptors, Leptin
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