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

Marcelo L G Correia; Kamal Rahmouni

doi:10.1111/j.1463-1326.2005.00562.x

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Journal article

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

Marcelo L G Correia and Kamal Rahmouni

Diabetes, obesity & metabolism, Vol.8(6), pp.603-610

11/2006

DOI: 10.1111/j.1463-1326.2005.00562.x

PMID: 17026484

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Abstract

To review the potential role of leptin, hyperleptinaemia and leptin resistance in the cardiovascular and endocrine complications of metabolic syndrome. Review of literature listed in Medline. 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 beta 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. Hyperleptinaemia and leptin resistance may contribute to hypertension, impaired glucose metabolism, and pro-atherogenic state in obesity and metabolic syndrome.

Leptin - physiology

Animals

Diabetes Mellitus, Type 2 - physiopathology

Leptin - blood

Atherosclerosis - physiopathology

Humans

Insulin Resistance

Metabolic Syndrome - physiopathology

Obesity - physiopathology

Blood Pressure - physiology

Drug Resistance

Hypertension - physiopathology

Details

Title: Subtitle: Role of leptin in the cardiovascular and endocrine complications of metabolic syndrome
Creators: Marcelo L G Correia - Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. marcelo-correia@uiowa.edu
Kamal Rahmouni
Resource Type: Journal article
Publication Details: Diabetes, obesity & metabolism, Vol.8(6), pp.603-610
DOI: 10.1111/j.1463-1326.2005.00562.x
PMID: 17026484
NLM abbreviation: Diabetes Obes Metab
ISSN: 1462-8902
eISSN: 1463-1326
Publisher: England
Language: English
Date published: 11/2006
Academic Unit: Iowa Neuroscience Institute; Neuroscience and Pharmacology; Endocrinology and Metabolism; Internal Medicine
Record Identifier: 9984040303502771

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