The Effects of Growth Hormone on the Utilization of L-Leucine in Adipose Tissue*

Abstract

Growth hormone [GH] (1 .mu.g/ml) increased the oxidation of L-[1-14C]leucine to 14CO2 in adipose tissue of hypophysectomized rats whether or not glucose was also present. Glucose alone also increased the rate of leucine consumption, and the magnitude of the GH effect was greater when glucose was also present. The stimulation of leucine oxidation by GH required a lag peirod of the order of 30 min, was maximal between 30 and 90 min, and thereafter declined and disappeared by 180 min. Addition of actinomycin D or cycloheximide along with GH caused the accelerated rate of leucine consumption to persist through at least the 4th h. After the response to GH had disappeared, the tissues were refractory to renewed stimulation with additional GH. GH produced comparable effects on the consumption of .alpha.-ketoisocaproate, the deaminated product of leucine, suggesting that the site of stimulation is distal to the transamination reaction. In the absence of glucose, GH failed to alter the rate of consumption of isovalerate, the next metabolite in the degradative pathway, suggesting that the site of stimulation precedes the appearance of this metabolite, and hence may be at the level of .alpha.-ketoisocaproate decarboxylation. Treatment of rats in vivo with 250 .mu.g/day of GH for 3 days decreased the utilization of L-[2-14C]leucine and [1-14C]isovalerate, but only when measured in the presence of glucose. This regimen of GH treatment had no effect on the rate of consumption of either substrate studied in the absence of glucose, suggesting that long term effects of GH on leucine consumption are indirect and secondary to the well known inhibition of glucose metabolism.