Type 1 diabetes (T1DM) is a disease characterized by autoimmune mediated destruction of the insulin
producing beta cells of endocrine pancreas. Beside insulin deficiency, T1DM is also characterized by abnormal
suppression of glucagon secretion in response to hyperglycemia. All these abnormalities are likely to leave patients
dependent upon exogenous insulin administration for survival. GLP-1 is a hormone secreted by L-cells of distal
small intestine and colon. GLP-1 exerts its effects through the interaction with GLP-1 receptor expressed in the
pancreatic islets, lung, hypothalamus, stomach, heart and kidney. It belongs to the group of incretin peptides and it
stimulates insulin and inhibits glucagon secretion. Actions of GLP-1 also include delaying of gastric emptying, reduction
of appetite and induction of satiety. On the other hand, evidences mainly collected from animal models,
have indicated the role of GLP-1 in increasing beta cell proliferation and differentiation and in decreasing the rate of beta cell apoptosis.
GLP-1 receptor agonists are approved for the treatment of type 2 diabetes where they have established very important position. However,
they are still not approved for use in T1DM, although they could have beneficial effects in both new onset and longstanding T1DM patients,
mainly as an adjunctive therapy to insulin in order to improve glycemic control and body weight management in longstanding disease
or to reduce insulin requirements or even to delay the absolute dependence upon insulin administration in new onset T1DM. Randomized,
long-term, placebo controlled clinical trials are warranted before the official implementation of GLP-1 receptor agonists in the
treatment of T1DM.
Keywords: Type 1 diabetes, glucagon-like peptide-1, pancreatic beta cells, insulin, glucagon, glycemic control, exenatide, liraglutide.
Rights & PermissionsPrintExport