[Effects of creatine phosphokinase competitive inhibitor on system and tissue energy metabolism in rats in the norm and during unloading].

In an experiment with rats system and intracellular energy metabolism was assessed by cell reactions to chronic injection of beta-guanidine propionic acid (beta-GPA) stimulating AMP-dependent protein kinase (AMPK). Suspension was shown to inhibit the succinate dehydrogenase (SDH) activity, reduce glycogen in both types of muscle fibers, and stimulate the activity of alpha-glycerophosphate dehydrogenase (alpha-GPDH) in fast fibers. Supplementing the rat chow with beta-GPA did not modify these parameters during suspension; however, the blood urea level increased considerably in the suspended and control rats. In the controls, beta-GPA as well as suspension, stimulates growth of the aspartate aminotranspherase activity (AST) in blood. Yet, the suspension and beta-GPA injection had no additive effect. Moreover, their effects were opposite in rats subjected to suspension + beta-GPA. Glucose concentration was observed to become lowered in blood of resting rats treated with beta-GPA. This effect can be associated with a more intensive insulin-dependent glucose transport to muscles. The additional glucose, because of increased demand by fibers, underwent to oxidation and did not replenish the intracellular carbohydrate deposits These data suggest energy metabolism shifting toward activation of the processes of disintegration of substrates for energy production due to a sharp growth of energy demand.