DPP-4 inhibitors may also enhance beta cell function in patients with type 2 diabetes mellitus.
Drugs that inhibit dipeptidyl peptidase-4 (DPP-4) act to preserve the levels of intact glucagon-like peptide-1 and glucose-dependent insulinotropic peptide.
An increase in these gut-derived incretin hormones following a meal is thought to be the predominant mechanism of action for these drugs.
But recent studies have found that they can also directly enhance insulin secretion from the pancreas.
A team of researchers in Australia and Germany, in an abstract to be presented June 7 at the 2015 American Diabetes Association annual meeting in Boston, MA, tested whether enteric glucose was required for inhibition of DPP-4 to enhance insulin secretion in type 2 diabetes.
Using a mouse strain bred to be obese and insulin resistant, the researchers treated the mice with linagliptin (Tradjenta/Boehringer Ingelheim).
“These enhancements in glucose stimulated insulin levels were not associated with an increase I beta cell mass,” they found. Their finding has promise for type 2 diabetes, they wrote.
“We conclude that DPP4 inhibition-mediated improvements in beta cell function do not require enteric glucose and suggest that direct effects of DPP4 inhibition on pancreatic islets may contribute to their action in this model of type 2 diabetes.”