The role of incretins in cardiovascular control

Glucagon-like peptide-1 (GLP-1) is an incretin secreted in response to nutrient ingestion. Understanding the incretin effect on diabetes pathophysiology has led to development of a new class of agents termed incretin mimetics. Exenatide is the first GLP-1 agonist approved to treat type 2 diabetes me...

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Bibliographic Details
Published in:Current hypertension reports 2009-02, Vol.11 (1), p.18-22
Main Authors: Mafong, Derek D., Henry, Robert R.
Format: Article
Language:English
Subjects:
Cardiology
Cardiovascular Agents - pharmacology
Cardiovascular System - drug effects
Cardiovascular System - physiopathology
Diabetes
Diabetes Mellitus, Type 2 - physiopathology
Family Medicine
General Practice
Human subjects
Humans
Hypertension
Incretins - physiology
Internal Medicine
Medical research
Medicine
Medicine & Public Health
Metabolic Diseases
Nephrology
Peptides - pharmacology
Primary Care Medicine
Venoms - pharmacology
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Summary:Glucagon-like peptide-1 (GLP-1) is an incretin secreted in response to nutrient ingestion. Understanding the incretin effect on diabetes pathophysiology has led to development of a new class of agents termed incretin mimetics. Exenatide is the first GLP-1 agonist approved to treat type 2 diabetes mellitus (T2DM). Clinical studies have demonstrated exenatide’s efficacy in improving glycemic control, often coupled with weight loss. Studies are investigating the potential cardiovascular benefits of GLP-1 agonists. Blood pressure, cholesterol levels, C-reactive protein, and insulin resistance may improve in patients treated with exenatide. The direct effect of GLP-1 on cardiac myocytes and vascular smooth muscle has been an active area of investigation. Infusions of GLP-1 in animal models and human subjects with heart failure have demonstrated significantly improved cardia parameters. In patients with T2DM, GLP-1 infusion has been shown to improve endothelial function, irrespective of changes in insulin sensitivity. These pilot studies provide a foundation for developing therapies aimed at modulating incretin physiology for the additional benefit on the cardiovascular system in patients with T2DM and heart disease.
ISSN:1522-6417
1534-3111
DOI:10.1007/s11906-009-0005-x