Effects of hypo- and hyperthyroidism on rat liver microsomal long-chain fatty acyl-CoA synthetase and hydrolase

The effects of hyperthyroidism (hyperT3), (tri-iodothryonine (T3) injected rats), and hypothyroidism (hypoT3) (thyroidectomized rats) on the activation of fatty acids by a microsomal long-chain fatty acyl-CoA (LCA-CoA) synthetase and the degradation of LCA-CoA by a microsomal LCA-CoA hydrolase was determined. MAS was assayed by measuring the [1-14C]-palmitate or -1-14C] oleate incorporated into its water soluble CoA ester. MAH was assayed spectrophotomerically by following the reduction of 5',5'-dithiobis-(2-nitrobenzoic acid) by the CoA released from palmitoyl-CoA or oleoyl-CoA. Enzyme activities are given as mean (nmoles/mg/min) +/- SEM. MAS activities were decreased 36-44% (p < 0.01) in both hypoT3 and hyperT3 (controls = 101 +/- 4 (n = 11, [1-14C]-palmitate) of 72 +/- 2 (n = 5,[1-14C]oleate)). These decreases may contribute to the decreased triacelyglycerol (TG) and phospholipid contents in the hyperT3 liver and the decreased clearance rate of plasma TG in the hypoT3. MAH was decreased 27-42% (p<0.01) only in hypoT3 (controls = 77 +/- 3 (n = 11, palmitoyl-CoA) or 45 +/- 1 (n = 5, oleoyl-CoA)). This decrease was corrected by T3 treatment. Since the decreased MAH would increase the availability of LCA-CoA, it may contribute to the increased TG synthesis in hypoT3