Combined treatment with a dipeptidyl peptidase-IV inhibitor (sitagliptin) and an angiotensin II type 1 receptor blocker (losartan) promotes islet regeneration via enhanced differentiation of pancreatic progenitor cells

Diabetes Obes Metab. 2012 Sep;14(9):842-51. doi: 10.1111/j.1463-1326.2012.01612.x. Epub 2012 May 8.

Abstract

Aim: The existence of pancreatic progenitor cells (PPCs) with differentiation capacity in the adult pancreas has rendered that promotion of islet regeneration is feasible. The dipeptidyl peptidase-IV inhibitor sitagliptin and the angiotensin II type 1 receptor (AT(1) receptor) blocker losartan have a common target action in the pancreata. Thus, we evaluated the synergistic/additive effects of these two drugs on the differentiation of islet progenitors.

Methods: The acute and chronic effects of sitagliptin and losartan, individually or in combination, on islet regeneration in vivo were investigated by using a streptozotocin-induced type 1 diabetes mouse model. Their effects were also examined on an in vitro PPCs model derived from human foetal pancreas.

Results: A chronic combination treatment enhanced glucose tolerance in diabetic mice associated with an increased ratio of β cells to islet; an acute combination treatment resulted in a marked increase in the production of neurogenin 3 (NGN3(+)) cells in proximity to CK7(+) ductal cell and an increased presence of insulin(+) /CK7(+) cells. The in vitro study revealed that a combination treatment significantly enhanced mRNA expression of NGN3, NKX6.1 and PDX-1 during PPCs differentiation into human islet-like cell clusters (ICCs). Despite no apparent changes in insulin release, the combined treatment resulted in increasing production of peroxisome proliferator-activated receptor γ (PPARγ) during PPC differentiation.

Conclusions: These data indicate that combined sitagliptin-losartan treatment can improve islet function by promoting the differentiation of PPCs into ICCs, perhaps via a mechanism involving PPARγ production, and could thereby, contribute to islet regeneration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II Type 1 Receptor Blockers / pharmacology*
  • Animals
  • Cell Differentiation
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / pathology
  • Dipeptidyl-Peptidase IV Inhibitors / pharmacology*
  • Drug Synergism
  • Humans
  • Islets of Langerhans / pathology
  • Islets of Langerhans / physiology*
  • Losartan / pharmacology*
  • Male
  • Mice
  • Pyrazines / pharmacology*
  • Regeneration / drug effects*
  • Sitagliptin Phosphate
  • Stem Cells / pathology
  • Triazoles / pharmacology*

Substances

  • Angiotensin II Type 1 Receptor Blockers
  • Dipeptidyl-Peptidase IV Inhibitors
  • Pyrazines
  • Triazoles
  • Losartan
  • Sitagliptin Phosphate