GLUCOSE-HOMEOSTASIS AND SYMPATHOADRENAL ACTIVITY IN MERCAPTOACETATE-TREATED RATS

The effect of the fatty acid oxidation inhibitor, sodium mercaptoacetate (MA, 600 mu mol/kg) on peripheral energy substrate metabolism was investigated in rats with permanent heart catheters. Rats were either fed, 48-h food deprived, or exercising for 30 min. Before and after intravenous MA injection, stress-free blood samples were taken for measurement of blood glucose, plasma free fatty acids (FFA), insulin, epinephrine (E), and norepinephrine (NE) concentrations. In fed animals, MA increased blood glucose, plasma FFA, and NE and decreased insulin concentrations. Plasma E levels did not change. In 48-h-deprived animals, MA elevated low baseline glucose concentrations to levels observed in MA-treated fed animals. Plasma insulin concentrations decreased to almost undetectable levels. Plasma catecholamines and FFA were increased compared to fed rats. In exercising rats, MA caused an exaggerated increase of blood glucose and a pronounced reduction of plasma insulin without affecting exercise-induced FFA and catecholamine responses. The data revealed that the mechanisms that regulate blood glucose concentrations during MA treatment are dependent on the nutritional state and ambient energy expenditure.