Dang A Q, Faas F H, Carter W J
John L. McClellan Memorial Veterans Hospital, Little Rock, Arkansas.
Horm Metab Res. 1989 Jul;21(7):359-61. doi: 10.1055/s-2007-1009237.
The effects of T3 treatment and thyroidectomy on rat liver microsomal long-chain fatty acyl-CoA (LCFA-CoA) synthetase and LCFA-CoA hydrolase activities were determined. Hyperthyroid rats had a 36-42% decrease in LCFA-CoA synthetase with no change in hydrolase activity. This may contribute to the redirection of fatty acids from esterification to oxidation reactions in hyperthyroidism. Thyroidectomized rats had a 40-44% decrease in synthetase and a 27-42% decrease in LCFA-CoA hydrolase activity. The decrease in both LCFA-CoA synthetase and hydrolase activities in hypothyroidism may indicate that the LCFA-CoA turnover in this futile cycle is decreased in the liver.
测定了T3治疗和甲状腺切除对大鼠肝脏微粒体长链脂肪酰辅酶A（LCFA-CoA）合成酶及LCFA-CoA水解酶活性的影响。甲状腺功能亢进的大鼠，LCFA-CoA合成酶活性降低了36% - 42%，而水解酶活性没有变化。这可能有助于解释甲状腺功能亢进时脂肪酸从酯化反应转向氧化反应的重定向。甲状腺切除的大鼠，合成酶活性降低了40% - 44%，LCFA-CoA水解酶活性降低了27% - 42%。甲状腺功能减退时LCFA-CoA合成酶和水解酶活性均降低，这可能表明肝脏中这个无效循环的LCFA-CoA周转减少。
