Acute exposure to rosiglitazone does not affect glucose transport in intact human skeletal muscle

作者：Skrobuk Paulina; Kuoppamaaa Heidi; Hiukka Anne; Koistinen Heikki A^*

来源：Metabolism-Clinical and Experimental, 2010, 59(2): 224-230.

DOI：10.1016/j.metabol.2009.07.016

Thiazolidinediones (TZDs) such as rosiglitazone are widely used as antidiabetic drugs Animal studies suggest that TZDs may have direct metabolic actions in skeletal muscle Here, we examined if acute exposure to rosightazone stimulates glucose transport rate and affects proximal insulin signaling in isolated skeletal muscle strips from nondiabetic men Open muscle biopsies were obtained from musculus vastus lateral's from 15 nondiabetic men (50 +/- 3 years old, 269 +/- 1.1 kg/m(2)) Skeletal muscle strips were isolated and exposed to rosightazone (1 or 10 mu mol/L), 5-aminoimidazole-4-carboxamide 1-beta-D-ribonucleoside (1 mmol/L), insulin (120 nmol/L), or a combination of insulin (120 nmol/L) and rosightazone (10 mu mol/L) in vitro for 1 hour Glucose transport was analyzed by accumulation of intracellular 3-O-methyl [(3)H] glucose; phosphorylation of Akt-Ser(473) and Akt-Thr(308) and phosphorylation of acetyl coenzyine A carboxylase beta were determined using phosphospecific antibodies 5-Aminoimidazole-4-carboxamide 1-beta-D-ribonucleoside and insulin increased glucose transport rate 1.5-fold (P < .05) and 1.7-fold (P < .01) in isolated muscle strips, respectively Exposure to rosiglitazone transiently increased phosphorylation of acetyl coenzyme A carboxylase beta, with a maximum effect at IS minutes and return to baseline at 60 minutes However, rosightazone did not affect basal or insulin-stimulated glucose transport rate, or phosphorylation of Ak

• 出版日期2010-2
• 单位河北医科大学