Assessment of Effect of Starvation, Glucose, Fatty Acids and Hormones on α-Decarboxylation of Leucine in Skeletal Muscle of Rat

Abstract

The present investigations of rates of oxidation of [U-¹⁴C] or [1-¹⁴C]leucine by homogenates of gastrocnemius muscle of fed and starved rats have indicated that ¹⁴CO₂ production is mainly the result of α-decarboxylation of leucine in this tissue. This incomplete oxidation was not the result of impaired tricarboxylic acid cycle since the oxidation of palmitate proceeded to completion within the experimental conditions. In the subsequent studies, the effect of altered nutrition and metabolic factors on α-decarboxylation of leucine by gastrocnemius muscle homogenates was investigated. Starvation increased the rate of α-decarboxylation of leucine. Glucose or palmitate (C₁₆) added in physiological concentrations to the incubation medium were without effect on decarboxylation of leucine, but this reaction was stimulated by addition of 1 mM hexanoate (C₆) or octanoate (C₈) to the incubation medium. However, when fatty acid chain length was clongated to C₁₀ (decanoate), the stimulatory effect was not only abolished, but this fatty acid significantly inhibited the rate of leucine decarboxylation. Addition of insulin, epinephrine, glucagon and cyclic AMP within a wide range of concentrations to the incubation medium did not significantly affect the rate of decarboxylation of leucine. These studies indicate a complex interrelationship between the metabolism of leucine and that of fatty acids.