Cited by 218Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesHypothalamic control of reproductive hormones

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The Concept of Selective Leptin Resistance

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Correia, Marcelo L.G., Haynes, William G., Rahmouni, Kamal, Morgan, Donald A., Sivitz, William I., Mark, Allyn L.·2002·Diabetes

DOI 10.2337/diabetes.51.2.439

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Abstract

Leptin, a hormone secreted by adipose tissue, acts to inhibit appetite and promote metabolism, thereby reducing body weight. Leptin also increases sympathetic activity and arterial pressure. Several murine models of obesity, including agouti obese mice, exhibit resistance to the anorexic and weight-reducing effects of leptin. Hypertension in agouti mice has been attributed to hyperleptinemia. These observations pose a seeming paradox. If these mice are leptin-resistant, then how can leptin contribute to hypertension? We tested the novel hypothesis that these mice have selective leptin resistance, with preservation of the sympathoexcitatory action despite resistance to the weight-reducing actions. Leptin-induced decreases in food intake and body weight were less in agouti obese mice than in lean littermates. In contrast, leptin-induced increases in sympathetic nerve activity did not differ in obese and lean mice. These findings support the concept of selective leptin resistance, with resistance to the metabolic actions of leptin but preservation of the sympathoexcitatory actions. This finding may have potential implications for human obesity, which is associated with elevated plasma leptin and is thought to be a leptin-resistant state. If leptin resistance is selective in obese humans, then leptin could contribute to sympathetic overactivity and its adverse consequences in human obesity.

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Authors: Correia, M. L. G., Haynes, W. G., Rahmouni, K., Morgan, D. A., Sivitz, W. I., & Mark, A. L.
Affiliations: University of Iowa (US)
ORCID: Correia, Marcelo L.G.
Haynes, William G.
Rahmouni, Kamal
Morgan, Donald A.
Sivitz, William I.
Mark, Allyn L.
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2002-02-01
Volume: 51
Issue: 2
Pages: 439-442
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/diabetes.51.2.439
OpenAlex: W2099930994
Cited by: 218
References: 21
Citations by year: 2026: 2 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 3 · 2021: 8 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 7 · 2016: 8 · 2015: 6 · 2014: 13 · 2013: 13 · 2012: 8
FWCI: 5.57
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Diabetes (publishedVersion)
PubMed (publishedVersion)
Funders: U.S. Department of Veterans Affairs
American Heart Association
National Institutes of Health (5p50hl044546-05)
National Heart, Lung, and Blood Institute (HL-14388, HL-44546, P01HL014388)
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 resistance, leptin, obesity, sympathetic activity, hypertension, dietary intake, body weight, hyperleptinemia, appetite regulation, sympathetic hyperactivity
MeSH terms: Animals, Body Weight, Drug Resistance, Eating, Mice, Inbred Strains, Obesity, Reference Values, Sympathetic Nervous System, Leptin, Mice

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