Cited by 121Adipokines, Inflammation, and Metabolic DiseasesRegulation of Appetite and ObesityDiabetes, Cardiovascular Risks, and Lipoproteins

Role of leptin in the cardiovascular and endocrine complications of metabolic syndrome

Correia, Marcelo L. G., Rahmouni, Kamal·2006·Diabetes, Obesity and Metabolism

Abstract

Aim: To review the potential role of leptin, hyperleptinaemia and leptin resistance in the cardiovascular and endocrine complications of metabolic syndrome. Methods: Review of literature listed in Medline. Results: Hyperleptinaemia is common in obesity and reflects increased adiposity and leptin resistance. Nevertheless, leptin resistance may not be complete as several actions of leptin, such as cardiovascular sympatho‐activation, might be preserved in obese subjects known to be resistant to the metabolic effects of leptin (i.e. selective leptin resistance). Notably, the renal and sympathetic actions of leptin may play an important role in the pathogenesis of hypertension related to obesity and metabolic syndrome. Furthermore, the lipotoxic effect of leptin resistance may cause insulin resistance and β cell dysfunction, increasing the risk of type 2 diabetes. Leptin has also been shown to possess proliferative, pro‐inflammatory, pro‐thrombotic, and pro‐oxidative actions. Conclusion: Hyperleptinaemia and leptin resistance may contribute to hypertension, impaired glucose metabolism, and pro‐atherogenic state in obesity and metabolic syndrome.

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Crossref · 10.1111/j.1463-1326.2005.00562.x

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  • Leptin resistance in obesity is restricted to the metabolic actions of leptin, and impaired leptin signaling was observed in ventricular cardiomyocytes isolated from rats subjected to 10-wk dietary sucrose feeding to generate hyperleptinemia and insulin resistance.

    “It was also recently suggested that leptin resistance in obesity is restricted to the metabolic actions of leptin (62), and impaired leptin signaling was observed in one study using ventricular cardiomyocytes isolated from rats subjected to 10-wk dietary sucrose feeding to generate hyperleptinemia and insulin resistance (139).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [62]

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Authors
Correia, M. L. G., & Rahmouni, K.
Affiliations
University of Iowa (US)
Corresponding author
Correia, Marcelo L. G.
Venue
Diabetes, Obesity and Metabolism
Publisher
Wiley
Published
2006-02-07
Volume
8
Issue
6
Pages
603-610
ISSN
  • 1462-8902 (ISSN-L)
  • 1463-1326
OpenAlex
W1976610229
Cited by
121
References
56
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 4 · 2019: 1 · 2018: 3 · 2017: 4 · 2016: 8 · 2015: 2 · 2014: 7 · 2013: 6 · 2012: 7
FWCI
1.80
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes Obesity and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
leptin, hyperleptinemia, leptin resistance, metabolic syndrome, obesity, hypertension, cardiovascular complications, insulin resistance, beta-cell dysfunction, type 2 diabetes, atherosclerosis, inflammation, thrombosis, oxidative stress, sympathetic activation
MeSH terms
Animals, Blood Pressure, Diabetes Mellitus, Type 2, Drug Resistance, Humans, Hypertension, Insulin Resistance, Obesity, Leptin, Metabolic Syndrome, Atherosclerosis

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