Leptin and hyperleptinemia - from friend to foe for cardiovascular function

Ren, J

doi:10.1677/joe.0.1810001

Cited by 305Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesCardiovascular Disease and Adiposity

Leptin and hyperleptinemia - from friend to foe for cardiovascular function

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Ren, J·2004·Journal of Endocrinology

DOI 10.1677/joe.0.1810001

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Abstract

The obese gene product, leptin, plays a central role in food intake and energy metabolism. The physiological roles of leptin in human bodily function have been broadened over the past decade since leptin was first discovered in 1994. Evidence has suggested that leptin plays a specific role in the intricate cascade of cardiovascular events, in addition to its well-established metabolic effects. Leptin, a hormone linking adiposity and central nervous circuits to reduce appetite and enhance energy expenditure, has been shown to increase overall sympathetic nerve activity, facilitate glucose utilization and improve insulin sensitivity. In addition, leptin is capable of regulating cardiac and vascular contractility through a local nitric oxide-dependent mechanism. However, elevated plasma leptin levels or hyperleptinemia, have been demonstrated to correlate with hyperphagia, insulin resistance and other markers of the metabolic syndrome including obesity, hyperlipidemia and hypertension, independent of total adiposity. Elevated plasma leptin levels may be an independent risk factor for the development of cardiovascular disease. Although mechanisms leading to hyperleptinemia have not been well described, factors such as increased food intake and insulin resistance have been shown to rapidly enhance plasma leptin levels and subsequently tissue leptin resistance. These findings have prompted the speculation that leptin in the physiological range may serve as a physiological regulator of cardiovascular function whereas elevated plasma leptin levels may act as a pathophysiological trigger and/or marker for cardiovascular diseases due to tissue leptin resistance.

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The ob/ob mouse model is rather unique (plasma leptin levels are increased in almost all other obese rodent models and in humans) and may not precisely reflect the alterations observed in human obesity.
“In general, the ob/ob mouse model is rather unique (plasma leptin levels are increased in almost all other obese rodent models and in humans, Ref. 297) and may not precisely reflect the alterations observed in human obesity.”
From Cardiac remodeling in obesity (2008) · cites this paper as [297]

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Authors: Ren, J.
Affiliations: University of Wyoming (US)
Corresponding author: Ren, J
ORCID: Ren, J
Venue: Journal of Endocrinology
Publisher: Bioscientifica
Published: 2004-04-01
Volume: 181
Issue: 1
Pages: 1-10
ISSN: 0022-0795 (ISSN-L)
1479-6805
DOI: 10.1677/joe.0.1810001
OpenAlex: W2097827059
Cited by: 305
References: 97
Citations by year: 2026: 2 · 2025: 5 · 2024: 8 · 2023: 6 · 2022: 12 · 2021: 12 · 2020: 6 · 2019: 10 · 2018: 6 · 2017: 7 · 2016: 10 · 2015: 14 · 2014: 16 · 2013: 18 · 2012: 19
FWCI: 2.79
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Endocrinology (publishedVersion)
PubMed (publishedVersion)
Funders: American Diabetes Association
American Heart Association
National Institutes of Health
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 › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords: leptin, hyperleptinemia, cardiovascular disease, leptin resistance, insulin resistance, metabolic syndrome, obesity, hypertension, hyperlipidemia, sympathetic activity, insulin sensitivity, nitric oxide, cardiac contractility, vascular contractility, cardiovascular risk factors
MeSH terms: Appetite Regulation, Blood Glucose, Blood Pressure, Cardiovascular Diseases, Energy Metabolism, Heart Rate, Humans, Insulin, Obesity, Receptors, Cell Surface, Sympathetic Nervous System, Signal Transduction, Leptin, Receptors, Leptin

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Leptin and hyperleptinemia - from friend to foe for cardiovascular function

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