The effects of leptin on F-actin remodelling in type-I diabetes.

BACKGROUND: The aim of the current study is to investigate the effect of leptin on cytoskeleton structures in both in vivo and in vitro model of diabetes.

MATERIALS AND METHODS: For in vivo studies, leptin in different doses (240, and 480 mg/kg) was injected to the diabetic rats after one-week of Streptozotocin (STZ, 55 mg/kg) treatment. Leptin levels were analyzed in serum, liver, and pancreas samples. Hepatic and pancreatic F-and G- actin expressions were determined by Western blotting. For in vitro studies, hepatic and pancreatic primary cell lines were obtained from the control rats. To these cultures, STZ (15 and 30 mM), leptin (50, 60 and 100 ng/ml), and their combinations were applied for one, three, and four weeks. After the treatment period, F-actin was visualized by the Alexa-fluor fluorescent dye.

RESULTS: STZ decreased the G-actin in both tissues in vivo. However, leptin caused a dose-dependent increase in G-actin levels while F-actin decreased in both tissues. Moreover, leptin caused the perimembranous condensation of actin filaments and amelioration of F-actin structures in vivo. A dose-dependent corruption of F-actin filament structures was observed in leptin-treated primary cells in vitro, while STZ also caused corruption of these filaments. Co-exposure of STZ and leptin caused the amelioration of F-actin filaments, while the perimembranous condensation was also observed as was in vivo study.

CONCLUSIONS: Leptin therapy could be a candidate for diabetes, but it should not be ruled out as being important the severity of diabetes and leptin doses.