Improvement in glucose tolerance and skeletal muscle glucose transport in broiler chickens treated with PPAR agonist Troglitazone

Carbohydrate metabolism in chickens is character ized by hyperglycemia and insulin resistance compared to that observed in mammals. We previously reported that although gene of GLUT4 (an insulin-responsive glucose transporter ) is deficient in chickens (Seki et al., 2003), GLUT1 and GLUT8 are expressed, to a very small extent, in skeletal muscles (Kono et al., 2005). Fur thermore, it has been evidenced that glucose transpor t across the plasma membrane of skeletal muscles is stimulated by insulin injection in growing chicks (Tokushima et al., 2005). In the insulin-mediated glucose transport in mammals, peroxisome prolifer ator-activated receptor-gamma (PPAR ) plays a crucial role. The present study was under taken to assess the involvement of PPAR in the glucose toler ance and skeletal muscle glucose transport in chickens by using troglitazone, a PPAR agonist. Broiler chickens aged 1 to 2 week were orally administered with troglitazone (50 mg/kg body weight/day) 2 times a day for 17-22 days. Plasma glucose and NEFA concentr ations were decreased, to a small extent, by troglitazone administration for 22 days. In an oral glucose toler ance test, troglitazone suppressed an increase in plasma glucose concentr ations following glucose loading (2 g glucose/kg BW). A decrease in the plasma glucose concentration in insulin-injected (40 g/kg BW) chickens was par tly intensified by troglitazone administr ation for 22 days. Troglitazone administr ation for 17 days augmented insulin-mediated glucose transport, being determined by 2DG uptake, in skeletal muscles (extensor digitorum longus (EDL), pectoral superficialis and pectoral profundus) of chickens. These results suggest that PPAR is involved in the regulation of carbohydrate metabolism species-specific to chickens and troglitazone improves insulin resistance through modulation of skeletal muscle glucose transport.