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.
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Selective leptin resistance occurs in obesity.
“An intriguing aspect to consider with respect to the influence of leptin on the myocardium is the concept that selective leptin resistance occurs in obesity (60, 61, 222, 223).”
From Cardiac remodeling in obesity (2008) · cites this paper as [223]
Initial studies suggested that while the effects of leptin on satiety and energy metabolism were resistant, the sympathoexcitatory effects were maintained.
“Initial studies purporting this concept suggested that while the effects of leptin on satiety and energy metabolism were resistant, the sympathoexcitatory effects were maintained (60, 61, 222, 223, 290, 291).”
From Cardiac remodeling in obesity (2008) · cites this paper as [223]
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- 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 › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Pharmacology › 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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