Abstract
The objective of this study was to investigate the effect of various selenium (Se) status on glucose intolerance and pancreatic oxidative stress or the defense systems in Nagoya-Shibata-Yasuda (NSY) mice as the animal model for type 2 diabetes mellitus. To let the mice become Se-insufficient to Se-sufficient conditions, the NSY mice were given normal or Se-deficient diet with 0-7.0 mg/l Na2SeO3-containing drinking water for 6, 8 or 12 weeks. In NSY mice ingested normal diet, levels of blood glucose and plasma insulin after intraperitoneal glucose tolerance test (IPGTT) were not significantly affected by Na2SeO3-supplementation. In Se-deficient diet-treatment groups, however, the supplementation resulted in the decrease of blood glucose and the increase of plasma insulin after IPGTT. Although glutathione peroxidase (GPX) 1 activity in pancreas of the NSY mice ingested Se-deficient diet was augmented by Na2SeO3-supplementation, pancreatic glutathione was depressed by the supplementation, accompanying by the increase of 2-thiobarbituric acid-reactive substances. These results indicated that although the supplemented Na2SeO3 may not protect against oxidative stress in the pancreas of NSY mice under Se-insufficient condition, the Se compound improved glucose intolerance of the mice.
