Type 2 diabetes is characterized by high plasma glucose levels, insulin resistance, and inadequate insulin production. Insulin is secreted by pancreatic beta islets and the number of beta islets strongly influences the body’s ability to process glucose.
In this issue of the Journal of Clinical Investigation, Walter Wahli and colleagues at the University of Lausanne report that PPARbeta/delta, a protein that regulates gene expression, is a critical mediator of beta islet insulin secretion in mice.
PPARbeta/delta-mutant mice had more beta islets and enhanced insulin secretion compared to normal mice. By examining the genes that were expressed in normal and mutant beta islets, Wahli and colleagues found that PPARbeta/delta represses genes that help beta islets secrete insulin. Further, islets lacking PPARbeta/delta released insulin more quickly than normal islets, suggesting that therapeutics targeting PPARbeta/delta in the pancreas may help stimulate insulin release in diabetic patients.
PPARβ/δ affects pancreatic β-cell mass and insulin secretion in mice
Center for Integrative Genomics, National Research Center Frontiers in Gene, Lausanne, UNK, CHE