Landriscina C, Gnoni G V, Quagliariello E
Eur J Biochem. 1976 Dec;71(1):135-43. doi: 10.1111/j.1432-1033.1976.tb11099.x.
Evidence is presented that rat liver microsomal fatty acid chain elongation synthesis and desaturation, as well as acetyl-CoA carboxylase and fatty acid synthetase, are strongly influenced by thyroid hormone level. Conversely, the fatty acid chain elongation system in mitochondria, unlike the oxidative capacity of palmitate, NADH, succinate and malate, does not seem significantly affected by the thyrotoxic state. In triiodothyronine-induced or thyroxine-induced hyperthyroidism, rat liver acetyl-CoA carboxylase, fatty acid synthetase and microsomal chain elongation and desaturation reactions are not greatly affected after the first 10 days of treatment, while after longer intervals a respective increase in these activities is shown of up to 87, 116 and 65% after 22 days. In propylthiouracil-induced hypothyroidism, all the above synthetic activities are strongly reduced immediately after three days of drug administration and diminished no further following longer periods. Although the pattern of synthesized fatty acids in the thyrotoxic state is similar to that obtained from normal subcellular rat fractions, the esterification process of fatty acids in microsomal lipids appears to be slightly inhibited in hypothyroid rats and increased following triiodothyronine or thyroxine administration. Finally, a reduction in the hepatic cyclic AMP level of about 41% is reported after 19 days of triiodothyronine-administration to rats. On the basis of the observed insensitivity of the mitochondrial fatty acid chain elongation system to the thyrotoxic state, a tentative interpretation of its role in the hepatic cell is postulated.
有证据表明，大鼠肝脏微粒体脂肪酸链延长合成与去饱和作用，以及乙酰辅酶A羧化酶和脂肪酸合成酶，均受到甲状腺激素水平的强烈影响。相反，线粒体中的脂肪酸链延长系统，与棕榈酸、NADH、琥珀酸和苹果酸的氧化能力不同，似乎不受甲状腺毒症状态的显著影响。在三碘甲状腺原氨酸诱导或甲状腺素诱导的甲状腺功能亢进中，大鼠肝脏乙酰辅酶A羧化酶、脂肪酸合成酶以及微粒体链延长和去饱和反应在治疗的前10天内影响不大，而在更长时间后，这些活性在22天后分别增加高达87%、116%和65%。在丙硫氧嘧啶诱导的甲状腺功能减退中，给药三天后上述所有合成活性立即大幅降低，且在更长时间后不再进一步降低。虽然甲状腺毒症状态下合成脂肪酸的模式与从正常大鼠亚细胞组分中获得的模式相似，但甲状腺功能减退大鼠微粒体脂质中脂肪酸的酯化过程似乎略有抑制，而在给予三碘甲状腺原氨酸或甲状腺素后有所增加。最后，据报道，给大鼠注射三碘甲状腺原氨酸19天后，肝脏环磷酸腺苷水平降低约41%。基于观察到的线粒体脂肪酸链延长系统对甲状腺毒症状态不敏感，推测了其在肝细胞中的作用。
