Cited by 215Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesPharmacology and Obesity Treatment

The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.

Selective leptin resistance: a new concept in leptin physiology with cardiovascular implications

Abstract

Leptin, an adipocyte secreted hormone, acts in the hypothalamus to inhibit appetite and promote thermogenic metabolism, thereby reducing adiposity and body weight. Leptin has multiple autonomic and cardiovascular actions, including sympathetic activation, increases in endothelium derived nitric oxide (NO), and angiogenesis. The predominant cardiovascular effect of chronic hyperleptinemia is a pressor effect mediated by increased sympathetic activity. The sympathetic and cardiovascular actions of leptin are discussed and evidence derived from studies of obese mice for the novel concept of selective leptin resistance is reviewed. This concept holds that in some obese states, there is preservation of the sympathoexcitatory actions of leptin despite resistance to the satiety and weight-reducing actions of the hormone. Selective leptin resistance might explain how hyperleptinemia could contribute to increases in sympathetic activity and arterial pressure in obese states where there is resistance to the metabolic (satiety and weight-reducing) actions of leptin. It is speculated here, that this concept may have potential implications for human obesity, which is often associated with elevated plasma leptin and partial resistance to the satiety effects of leptin. If selective leptin resistance occurs in obese humans, then leptin could contribute to the sympathetic overactivity and hypertension despite resistance to its metabolic actions.

Overview

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Crossref · 10.1097/00004872-200207000-00001

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46 of 46 references verified0 citation errors · 0 not checkable

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Citations

Cites

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Research works printed but not linked: 3

  1. Mountjoy, 1994, Mol Endocrinol, 8, 1298, 10.1210/me.8.10.1298 · DOI
  2. Morgan, 2001, Hypertens, 38, 478
  3. Landsberg, 1986, Q J Med, 236, 1081

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Metadata

Authors
Mark, A. L., Correia, M. L. G., Rahmouni, K., & Haynes, W. G.
Affiliations
  • University of Iowa (US)
  • Universidade do Estado do Rio de Janeiro (BR)
Corresponding author
Mark, Allyn L.
Venue
Journal of Hypertension
Published
2002-07
Volume
20
Issue
7
Pages
1245-1250
ISSN
0263-6352 (ISSN-L)
OpenAlex
W1964056978
Cited by
215
References
45
Citations by year
2026: 1 · 2025: 6 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 3 · 2017: 10 · 2016: 6 · 2015: 9 · 2014: 14 · 2013: 7 · 2012: 7
FWCI
2.23
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p50hl044546-05)
  • National Heart, Lung, and Blood Institute (HL-44546)
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 › Pharmacology (medical) › Pharmacology and Obesity Treatment
Keywords
leptin, leptin resistance, hyperleptinemia, obesity, sympathetic nervous system, hypertension, satiety, thermogenesis, endothelial nitric oxide, angiogenesis, arterial pressure
MeSH terms
Animals, Appetite Regulation, Cardiovascular System, Drug Resistance, Humans, Obesity, Sympathetic Nervous System, Weight Loss, Leptin

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