Regulation of leptin production: sympathetic nervous system interactions

Rayner, D. Vernon; Trayhurn, Paul

doi:10.1007/s001090100198

Cited by 250Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and Metabolism

Regulation of leptin production: sympathetic nervous system interactions

Rayner, D. Vernon, Trayhurn, Paul·2001·Journal of Molecular Medicine

DOI 10.1007/s001090100198

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Abstract

Leptin is secreted primarily from white adipose tissue and stimulates long-form OB-Rb receptors in the hypothalamus to decrease food intake and increase energy expenditure. A variety of neuropeptides are involved in these responses, including neuropeptide Y, agouti-related protein, the prepro-melanocortin system and cocaine- and amphetamine-regulated transcript. OB-Rb receptors (and other receptor isoforms) are also found in peripheral tissues. Leptin is now known to have a wide range of peripheral actions and is involved in activating the immune system, haematopoiesis, angiogenesis and as a growth factor, as well as being a regulator of many cellular functions. The identification of leptin has led to reappraisal of the role of white adipose tissue from being an organ concerned primarily with energy storage as fat to an understanding that it is also a major endocrine and secretory organ. While the importance of the sympathetic nervous system in mobilising fatty acids from adipose tissue has long been known, it has become apparent that the sympathetic system is a key regulator of leptin production in white adipose tissue as well. Sympathomimetic amines and cold exposure or fasting (which lead to sympathetic stimulation of white fat), decrease leptin gene expression in the tissue and leptin production. On the other hand, sympathetic blockade often increases circulating leptin and leptin gene expression, and it is possible that the sympathetic system has a tonic inhibitory action on leptin synthesis. Apart from the few instances where leptin is absent, leptin levels are increased in obesity, while the sympathetic sensitivity of adipose tissue is reduced, consistent with the high leptin levels that are seen. The dysregulation of energy balance leading to obesity may partly involve a decrease in leptin sensitivity, or the leptin system may be set to have maximal effects at low leptin levels.

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Data suggest that the release of leptin and ghrelin may be influenced by the autonomic nervous system, with cholinergic (vagal) activity suppressing ghrelin secretion and sympathetic activity decreasing leptin production.
“Data also exist suggesting that the release of these hormones may be influenced by the autonomic nervous system, with cholinergic (vagal) activity suppressing ghrelin secretion and sympathetic activity decreasing leptin production.62,63”
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 [63]
Leptin secretion is inhibited by sympathetic activity and ghrelin secretion is inhibited by parasympathetic activity.
“Since leptin secretion is inhibited by sympathetic activity [65] and ghrelin secretion is inhibited by parasympathetic activity [66], the changes in the activity of autonomic nervous system observed with sleep loss may be involved in the simultaneous reduction of leptin and increase of ghrelin.”
From Role of sleep duration in the regulation of glucose metabolism and appetite (2010) · cites this paper as [65]

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Authors: Rayner, D. V., & Trayhurn, P.
Affiliations: University of Aberdeen (GB)
University of Oslo (NO)
ORCID: Trayhurn, Paul
Venue: Journal of Molecular Medicine
Publisher: Springer Science and Business Media LLC
Published: 2001-02-20
Volume: 79
Issue: 1
Pages: 8-20
ISSN: 0946-2716 (ISSN-L)
1432-1440
DOI: 10.1007/s001090100198
OpenAlex: W2154900520
Cited by: 250
References: 182
Citations by year: 2026: 2 · 2025: 5 · 2024: 9 · 2023: 7 · 2022: 3 · 2021: 6 · 2020: 3 · 2019: 6 · 2018: 3 · 2017: 3 · 2016: 9 · 2015: 8 · 2014: 11 · 2013: 11 · 2012: 9
FWCI: 5.34
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Journal of Molecular Medicine (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 › Physiology › Adipose Tissue and Metabolism
Keywords: leptin, sympathetic nervous system, white adipose tissue, leptin gene expression, neuropeptides, neuropeptide Y, agouti-related protein, cocaine- and amphetamine-regulated transcript, sympathetic nerve block, cold exposure, fasting, obesity, leptin resistance, energy balance, adipose tissue endocrine function
MeSH terms: Adipose Tissue, Energy Metabolism, Models, Biological, Obesity, Research Personnel, Sympathetic Nervous System, Leptin

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Regulation of leptin production: sympathetic nervous system interactions

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