Myocardial infarction is sufficient to increase GLP-1 secretion leading to improved left ventricular contractility and mitochondrial respiratory capacity
Diabetes, Obesity and Metabolism Aug 04, 2018
Diebold S, et al. - Researchers evaluated circulating concentrations of GLP-1 (an incretin hormone with glucoregulatory and cardioprotective capacities secreted in response to nutritional and inflammatory stimuli) following myocardial infarction and its functional relevance regarding metabolism, left ventricular contractility and mitochondrial function. Patients with acute myocardial infarction showed clearly increased circulating GLP-1 concentrations. In an experimental model, myocardial infarction by permanent LAD ligation led to an increase in GLP-1 secretion in a time dependent manner, which coincided with the capacity of DPP-4 inhibition (by Linagliptin) to augment left ventricular contractility in a GLP-1 receptor dependent manner. AMPK activity increased and mitochondrial respiratory capacity of non-infarcted tissue areas was stimulated with DPP-4 inhibition. For left ventricular contractility during myocardial infarction, this study emphasizes a new functional relevance of inflammatory GLP-1 secretion.
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