Pulmonary and hepatic fatty acid synthesis. III. Control of hexose monophosphate shunt pathway by 3,5,3'-L-triiodothyronine.

Abstract

The hexose monophosphate shunt (HMPS) pathway activities were measured in lung and liver by estimating the relative conversion of [1-14C]-glucose and [6-14C]-glucose into 14CO2 as well as by assaying the glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities. The HMPS activities were depressed in the livers of diabetic and hypophysectomized rats and enhanced by 3,5,3'-L-triiodothyronine (T3) or insulin. The hepatic HMPS activities were stimulated to supranormal levels when normal rats were injected with T3. T3-mediated stimulation of hepatic enzyme activities was dependent on the dose and duration of the hormonal treatment. Half-lives of T3-induced synthesis and degradation of glucose 6-phosphate dehydrogenase were 20 and 96 h, respectively, and of 6-phosphogluconate dehydrogenase were 19 and 90 h, respectively. Although HMPS activity was found in lung, the activities of the HMPS pathway dehydrogenase did not vary with the alteration of hormonal conditions, nor the activities were stimulated by the action of T3 or insulin.