Glucagon-like peptide 1: continued advances, new targets and expanding promise as a model therapeutic

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Abstract
This article discusses glucagon-like peptide 1 physiology and its various sites of action beyond the incretin effect and highlights recent findings (2005 and 2006). Glucagon-like peptide 1 is a physiological incretin in humans and promotes insulin secretion after nutrient ingestion. It is secreted from intestinal L cells after meals and may be partially responsible for the improved glycemic control and weight loss after bariatric surgery. In vivo, glucagon-like peptide 1 is quickly degraded by dipetidyl peptidase IV to glucagon-like peptide 1(9-36), which has unclear physiologic activity. Glucagon-like peptide 1 and its specific receptor are also expressed in the brain, and central nervous system. Glucagon-like peptide 1 can reduce food intake, mediate toxic illness responses and control muscle and liver glucose disposal. In the heart, glucagon-like peptide 1 receptor activation improves cardiac hemodynamics in patients following angioplasty and has a beneficial effect on myocardial function in heart failure and postischemic animal models. Finally, glucagon-like peptide 1 augments islet mass and recent studies have identified cellular mechanisms by which glucagon-like peptide 1 receptor signaling affects this process. Glucagon-like peptide 1 is emerging as a regulatory factor with a broad range of actions related to substrate and energy metabolism. With the recent development of medications based on glucagon-like peptide 1 receptor signaling for diabetes treatment, these new findings suggest the promise of further application of this system for the treatment of other conditions such as obesity and cardiovascular disease.