| The whole body UCP2 knockout (UCP2-/-) have enhanced insulin secretion and higher ATP content. However, these changes could be due to indirect effects of extra-pancreatic deletion and therefore, generating beta-cell specific knockout mice (UCP2BKO) is essential. A 90% knockdown of UCP2 protein was observed in beta-cells of UCP2BKO mice. No significant differences were observed in body weight accumulation, fasting blood glucose, plasma insulin or glucagon. UCP2BKO had impaired oral glucose tolerance with no differences in insulin secretion or sensitivity. Enhanced ROS accumulation was observed in the beta-cells of UCP2BKO and upregulation of antioxidant enzyme genes. Morphometric analysis showed an increased glucagon positive area in the pancreata of UCP2BKO mice. Results obtained from UCP2BKO were contrary to the phenotype observed in UCP2-/- mice. Overall, the characterization of UCP2BKO demonstrates that UCP2 in the beta-cell is involved in modulating ROS production. |
