Adrenaline action in normal and insulin-resistant Zucker rat skeletal muscles : Effect on insulin-stimulated glucose uptake and glycogen breakdown

Abstract

Abstract

Carbohydrates are the major source of energy for most humans and account for about 60% of the energy consumed. In the human body carbohydrates are stored as glycogen in the liver and in the skeletal muscles. Regulation of glycogen synthesis is of great importance in the process of blood glucose homeostasis as glucose is stored as glycogen. Insulin and adrenaline are the most important hormones which regulate glycogen breakdown and glucose uptake. Adrenaline normally contrasts the effect of insulin in metabolic regulation. Insulin stimulates glucose uptake and synthesis of glycogen and lipids leading to energy accumulation whereas adrenaline decreases insulin-stimulated glucose uptake, increases energy expenditure and stimulates breakdown of glycogen and lipids. The aim of this study was to investigate the effect of adrenaline on insulin-stimulated glucose uptake and glycogen breakdown in soleus and EDL muscles from lean and insulin resistant obese Zucker rat. Experiments were done in vitro, as muscles were surgically removed from rats and incubated with insulin, adrenaline or insulin and adrenaline together. Other muscles were stimulated electrically. Glucose uptake was calculated from the intracellular accumulation of ³H-deoxy-D-glucose during incubation while glycogen content was measured through hydrolyzing of glycogen with amyloglucosidase. The formed glucose measured indirectly by measuring the amount of hexokinase and glucose-6-phosphate dehydrogenase fluorometrically. In this study my results showed that adrenaline decreased insulin-stimulated glucose uptake in soleus and EDL muscles from lean and obese Zucker rats. Adrenaline was without effect on basal glucose uptake in soleus muscles from lean and obese Zucker rats. We found also that, glycogen content was higher in soleus muscles from obese Zucker rats than in soleus muscles from lean littermates in control rested state and after exposure to adrenaline. Adrenaline stimulated glycogen breakdown in insulin resistant EDL muscles but not in normal muscles. In conclusion, adrenaline decreased insulin-stimulated glucose uptake in both normal and insulin resistant muscles. Furthermore adrenaline stimulated glycogen breakdown in EDL but not soleus muscles from obese Zucker rats. This suggests that β-adrenergic signaling is not impaired in insulin resistant muscles.