Vladimír Uličiansky, Zbynek Schroner
Liraglutide- new acylated, long-acting glucagon-like peptid-1 (GLP-1) analog is non-covalently binded by fatty acid to albumin. This strong binding to serum albumin, modification of the molecule and spontaneous aggregation of liraglutide molecules leads to inhibition of subcutaneous (s.c.) absorbtion, resistance to enzyme dipeptidyl peptidase-4 (DPP-4) and prolongation of the effect. Biological half-life is in the range of 10 - 15 hours and that’s why this compound is suitable for once-daily s.c. administration. At present liraglutide is undergoing late phases of clinical trials and its introducing to the market is expecting in near future. Beside the glucose dependent stimulation of insulin secretion, liraglutide supresses inappropriate postprandial glucagon secretion, only moderatly delays gastric emptying, by decreasing appetite reduces food intake. In clinical studies liraglutide improved markers of B-cells function (HOMA-B, the proinsulin/insulin ratio). In animal models of diabetes liraglutide increases number of B-cells by decreasing apoptosis and by stimulating neoproliferation of B-cells from cells of pancreatic ducts. Addition of liraglutide to the previous treatment is suitable mainly in obese patients with type 2 diabetes mellitus. It seems, that this preparation may have also potential to the decreasing of the incidence of cardiovascular events in type 2 diabetics.