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Editorials

GLP-1 Therapy

Beyond Glucose Control

Derek J. Hausenloy, MRCP, PhD and Derek M. Yellon, PhD, DSc, FRCP

From the Hatter Cardiovascular Institute, University College London Hospital and Medical School, London, United Kingdom.

Correspondence to Derek M. Yellon, PhD, DSc, FRCP, Hatter Cardiovascular Institute, University College London Hospital and Medical School, 67 Chenies Mews, London, WC1E 6HX, United Kingdom. E-mail hatterinstitute@ucl.ac.uk

Key Words: diabetes mellitus • heart failure • infarction • ischemia • reperfusion

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The number of diabetic patients is increasing at an alarming rate and, according to the World Health Organisation, is estimated to reach 300 million worldwide by the year 2025. Coronary heart disease is the leading cause of death in these patients. Diabetic patients are 2 to 3 times more likely to develop coronary heart disease, and they experience worse clinical outcomes after coronary artery angioplasty, cardiac bypass surgery, acute myocardial infarction, and the onset of cardiac failure. Clearly, new treatment strategies that are specifically directed to improving clinical outcomes in diabetic patients with coronary heart disease and in those patients who develop cardiac failure need to be developed.

Article 153

Emerging research studies suggest that newer antidiabetic therapies not only control glucose levels but also have an impact on cardiovascular disease. In this regard, glucagon-like peptide-1 (GLP-1), the synthetic analogue of which is already in clinical use as an antidiabetic therapy (exenatide), may exert beneficial cardiovascular effects independent of its glucose-lowering actions.¹ The active form of GLP-1 is the amide GLP-1(7-36), which is secreted by entero-endocrine L cells of the ileum and colon in response to a meal. GLP-1(7-36) reduces postprandial hyperglycemia and induces weight loss by stimulating insulin secretion from β cells in the pancreas (its incretin action), inhibiting glucagon secretion from pancreatic cells, inhibiting gastrointestinal secretion and motility, and causing satiety by acting on appetite-control centers in the brain (reviewed in reference ²). These GLP-1 effects are mediated by binding to the GLP-1 receptor, which is a G-coupled . . . [Full Text of this Article]