Cited by 516Adipokines, Inflammation, and Metabolic DiseasesRegulation of Appetite and ObesityCardiovascular Disease and Adiposity

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Leptin Resistance

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Martin, Seth S., Qasim, Atif, Reilly, Muredach P.·2008·Journal of the American College of Cardiology

DOI 10.1016/j.jacc.2008.05.060PMC PMC4556270

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Abstract

Leptin is an adipocyte-derived hormone and cytokine that regulates energy balance through a wide range of functions, including several that are important to cardiovascular health. Increased circulating leptin, a marker of leptin resistance, is common in obesity and independently associated with insulin resistance and cardiovascular disease (CVD) in humans. The mechanisms of leptin resistance include genetic mutation, leptin self-regulation, limited tissue access, and cellular or circulating molecular regulation. Evidence suggests that central leptin resistance causes obesity and that obesity-induced leptin resistance injures numerous peripheral tissues, including liver, pancreas, platelets, vasculature, and myocardium. This metabolic- and inflammatory-mediated injury may result from either resistance to leptin's action in selective tissues, or excess leptin action from adiposity-associated hyperleptinemia. In this sense, the term "leptin resistance" encompasses a complex pathophysiological phenomenon. The leptin axis has functional interactions with elements of metabolism, such as insulin, and inflammation, including mediators of innate immunity, such as interleukin-6. Leptin is even purported to physically interact with C-reactive protein, resulting in leptin resistance, which is particularly intriguing, given C-reactive protein's well-studied relationship to cardiovascular disease. Given that plasma levels of leptin and inflammatory markers are correlated and also predict cardiovascular risk, it is conceivable that part of this risk may be mediated through leptin resistance-related insulin resistance, chronic inflammation, type II diabetes, hypertension, atherothrombosis, and myocardial injury. Leptin resistance and its interactions with metabolic and inflammatory factors, therefore, represent potential novel diagnostic and therapeutic targets in obesity-related cardiovascular disease.

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Authors: Martin, S. S., Qasim, A., & Reilly, M. P.
Affiliations: University of Pennsylvania (US)
Corresponding author: Reilly, Muredach P.
ORCID: Martin, Seth S.
Qasim, Atif
Reilly, Muredach P.
Venue: Journal of the American College of Cardiology
Publisher: Elsevier BV
Published: 2008-10
Volume: 52
Issue: 15
Pages: 1201-1210
ISSN: 0735-1097 (ISSN-L)
DOI: 10.1016/j.jacc.2008.05.060
PMC: PMC4556270
OpenAlex: W102714011
Cited by: 516
References: 137
Citations by year: 2026: 14 · 2025: 22 · 2024: 19 · 2023: 21 · 2022: 18 · 2021: 35 · 2020: 32 · 2019: 23 · 2018: 26 · 2017: 34 · 2016: 31 · 2015: 37 · 2014: 34 · 2013: 38 · 2012: 31
FWCI: 3.60
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1749 d)
Locations: Journal of the American College of Cardiology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (R01DK071224)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords: leptin resistance, leptin, obesity, cardiovascular disease, insulin resistance, hyperleptinemia, chronic inflammation, interleukin-6, C-reactive protein, type 2 diabetes, hypertension, atherothrombosis, myocardial injury, energy balance, leptin signaling
MeSH terms: Animals, Cardiovascular Diseases, Humans, Inflammation, Obesity, Leptin

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