Favorable Glp Actions In Type Diabetes Beyond The Insulinotropic Effect

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GLP-1 inhibits glucagon secretion (32,33). In type 2 diabetes, excessive glucagon secretion in relation to the plasma glucose aggravates fasting hyperglycemia by stimulating hepatic glucose output (34). Exogenous administration of GLP-1 in type 2 diabetic patients leads to a significant suppression of glucagon secretion together with a normalization in fasting plasma glucose (29). The counterregulatory response of glucagon secretion in hypoglycemia is unaffected by GLP-1 administration (35). GLP-1-based therapies will therefore not bear an intrinsic risk for hypoglycemia (36).

Concerning gastrointestinal functions, GLP-1 slows gastric emptying and inhibits gastric acid secretion (18). In the central nervous system, GLP-1 acts as a neurotransmitter in the hypothalamus and stimulates satiety directly (37). Continuous GLP-1 application over 6 weeks in type 2 diabetic patients produced significant weight loss due to reduced food intake and increased satiety (37,38). Whether the effects of GLP-1 on satiety in humans are mainly mediated by the retardation of gastric emptying through a feedback loop or are centrally mediated is not completely clear yet (39,40).

In animal studies as well as in vitro studies including studies with human islets GLP-1 causes an increase of beta cell mass. This increase is explained by a stimulation of islet cell neogenesis (41-43) from precursor cells as well as an inhibition of apoptosis of beta cells (42,44). In man, the effect of GLP-1 on the beta cell mass cannot easily be quantified, but indirect measures of beta cell function have shown an improvement after GLP-1 application (45). in vitro, in isolated human islets, GLP-1 improves insulin secretion and islet cell morphology (46).

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