Horm Metab Res 2008; 40(9): 593-606
DOI: 10.1055/s-0028-1082326
Review

© Georg Thieme Verlag KG Stuttgart · New York

The Potential Beneficial Role of Glucagon-like Peptide-1 in Endothelial Dysfunction and Heart Failure Associated with Insulin Resistance

T. Nyström 1
  • 1Karolinska Institute, Department of Internal Medicine, Stockholm South Hospital, Stockholm, Sweden
Further Information

Publication History

received 05.10.2007

accepted 23.01.2008

Publication Date:
15 September 2008 (online)

Abstract

Endothelial dysfunction is a major characteristic of the atherosclerotic process and can be used to predict the outcome of cardiovascular disease in humans. Together with obesity and insulin resistance, such dysfunction is common among patients with type 2 diabetes and may explain their poor prognosis in connection with such a disease. Insulin resistance in skeletal muscle, adipose tissue, and the liver, a well-characterized feature of obesity and type 2 diabetes, contributes to the impairment of glucose homeostasis. Furthermore, the myocardial muscle can also be resistant to insulin, which might, at least in part, explain the frequent development of heart failure in individuals suffering from type 2 diabetes. The relationship between insulin resistance and endothelial dysfunction has prompted investigations, which reveal that regular exercise, dietary changes, and/or pharmacological agents can both increase insulin sensitivity and improve endothelial function. Glucagon-like peptide-1, an incretin, lowers blood levels of glucose and offers a promising new approach to the treatment of type 2 diabetes mellitus. Its extensive extra-pancreatic effects, including a favorable influence on cardiovascular parameters, are extremely interesting in this connection. The potential pharmacological effects of glucagon-like peptide-1 and its analogues on the endothelium and the heart are discussed in the present review.

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Correspondence

T. Nyström

Södersjukhuset

Ringvägen 52

118 83 Stockholm

Sweden

Phone: +46/8/6163 211

Fax: +46/8/6163 146

Email: thomas.nystrom@sodersjukhuset.se

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