抄録
Both uncoupling proteins, UCP2 and UCP3, show high homologies to UCP1, a mitochondrial carrier protein, which has been shown to play a role in the regulation of energy metabolism. UCP3 gene is expressed abundantly in the skeletal muscles while UCP2 gene is expressed in the white adipose cells in various tissues of the body. Based on their homologies to UCP1, UCP2 and UCP3 are believed to be involved in the regulation of energy balance. In this paper, we examined whether the expression of UCP2 and UCP3 is affected in obese and hyperglycemic mice, since obesity is associated with disturbed energy and glucose metabolism. We generated obese and hyperglycemic mice by using gold thioglucose (GTG) at the age of 6 weeks. Body weight were significantly increased at the age of 11, 16 and 26 weeks in GTG mice in comparison with control mice. Plasma glucose and insulin levels of GTG mice at the age of 11 weeks increased more than those of control mice. Pancreatic beta cell mass also increased significantly in GTG mice at the age of 16 weeks. We found that UCP2 mRNA levels in skeletal muscle of GTG mice were higher than those of control mice by 5.2-fold (16 weeks) and 2.9-fold (26 weeks), respectively. We also found that UCP3 mRNA levels in the skeltal muscle of GTG mice were higher than those of control mice by 2.7-fold (16 weeks) and 2.3-fold (26 weeks), respecively. Thus, the present study supports the concept that UCP2 and UCP3 may profoundly contribute to improvement of obesity and glucose metabolism in GTG induced obese mice via thrifty effects on heat production.
