A significant contributing factor to type II diabetes is islet β-cell dysfunction. Treatment of diabetes, hypertension, and heart disease with the angiotensin II receptor blockers (ARB) has shown some protection against the gradual loss of pancreatic function. Recent studies have also shown that extending the lifetime of the glucagon-like peptide-1 via inhibition of it degradation, with a dipeptidyl peptidase-IV inhibitor, also protects against loss of β-cell integrity and improves glucose-stimulated insulin secretion. Because the ARB and peptidase inhibitors act via disparate pathways, it is possible that they could be synergistic in the protection of islet function, and this is the conclusion of a study by Cheng et al. in this issue. Combination treatment of db/db diabetic mice with valsartan and LAF237 [(S)-1-[(3-hydroxy-1-adamantyl)ammo]acetyl-2-cyano-pyrrolidine], a peptidase inhibitor, demonstrated synergistic improvement in islet β-cell area and proliferation along with reduced oxidative stress and fibrosis.
See article at J Pharmacol Exp Ther 2008, 327:683–691.
- The American Society for Pharmacology and Experimental Therapeutics