Abstract
GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), which are released from the intestines after meals, are responsible for augmenting insulin secretion (ie, the incretin effect). Because the insulinotropic effect of GIP is markedly attenuated in type 2 diabetes, therapeutic development to date has focused on GLP-1, which also lowers blood glucose by suppressing glucagon and energy intake, and slowing gastric emptying.1 Use of GLP-1 receptor agonists for the management of type 2 diabetes is increasing rapidly, and is associated with weight loss, negligible risk of hypoglycaemia, and potential cardiovascular protection.
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