GLUCOSE-HOMEOSTASIS AND SYMPATHOADRENAL ACTIVITY IN MERCAPTOACETATE-TREATED RATS

The effect of the fatty acid oxidation inhibitor, sodium mercaptoaceta te (MA, 600 mu mol/kg) on peripheral energy substrate metabolism was i nvestigated in rats with permanent heart catheters. Rats were either f ed, 48-h food deprived, or exercising for 30 min. Before and after int ravenous MA injection, stress-free blood samples were taken for measur ement of blood glucose, plasma free fatty acids (FFA), insulin, epinep hrine (E), and norepinephrine (NE) concentrations. In fed animals, MA increased blood glucose, plasma FFA, and NE and decreased insulin conc entrations. 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 alm ost undetectable levels. Plasma catecholamines and FFA were increased compared to fed rats. In exercising rats, MA caused an exaggerated inc rease of blood glucose and a pronounced reduction of plasma insulin wi thout affecting exercise-induced FFA and catecholamine responses. The data revealed that the mechanisms that regulate blood glucose concentr ations during MA treatment are dependent on the nutritional state and ambient energy expenditure.