Enzyme Activities Related to Fatty‐Acid Synthesis in Liver and Adipose Tissue of Rats Treated with Triiodothyronine

Abstract

The effect of triiodothyronine treatment on fatty acid synthesis was investigated in liver and adipose tissue of fed and 48‐h fasted rats. In the liver, the thyrotoxic state was accompanied by an increased incorporation of [1‐14C]acetyl‐CoA to fatty acids and a rise in the activity of acetyl‐CoA carboxylase and fatty acid synthetase, both in the fed and fasted rats. The activity of glucose‐6‐phosphate dehydrogenase and 6‐phosphogluconate dehydrogenase, NADP‐malate dehydro‐genase and ATP citrate lyase was also enhanced by triiodothyronine treatment. Liver malate and citrate content was not changed in fed thyrotoxic rats, but was increased in fasted triiodo‐thyronine‐treated animals. Palmitate oxidation was increased in the liver of the same animals, either fed or fasted. The rise in acetyl‐CoA carboxylase activity due to triiodothyronine administration was apparent when assayed both before and after citrate activation in vitro. Maximal activity of this enzyme in the presence of citrate was reached earlier in the liver of triiodothyronine‐treated rats. In adipose tissue, triiodothyronine treatment induced an increase in the activity of acetyl‐CoA carboxylase, fatty acid synthetase and in glucose‐6‐phosphate dehydrogenase and 6‐phosphogluconate dehydrogenase. The activity of NADP‐malate dehydrogenase and ATP citrate lyase was slightly but insignificantly increased. Malate and citrate levels in adipose tissue were unchanged by triiodothyronine treatment. It is suggested that the triiodothyronine‐induced simultaneous stimulation of opposing pathways (the synthesis of fatty acids and their oxidation) creates a futile metabolic cycle which contributes to the general energy waste and thermogenesis characteristic of thyrotoxicosis. Copyright © 1972, Wiley Blackwell. All rights reserved