Objective The transcriptional coactivator PGC-1 α is an important factor regulating the expression of genes for oxidative phosphorylation in a number of tissues including skeletal muscle, liver and adipose tissue.Previous in vitro and in vivo studies using adenoviral mediated overexpression and shRNA approach showed that PGC-1 α suppressed beta-cell energy metabolism and negatively regulated insulin secretion, resulting in impaired glucose tolerance.By contrast, a recent study using isolated human islets showed that PGC-1 α promotes insulin secretion, and PGC-1 α expression in human islets is down-regulated in Type 2 diabetic patients.Our study is designed to determine the requirement for PGC-1 α in regulating beta-cell function using beta-cell selective PGC-1 α knockout mice.