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甲状腺激素对脂肪生成的调节及其在产热中的作用。

The regulation of lipogenesis by thyroid hormone and its contribution to thermogenesis.

作者信息

Freake H C, Schwartz H L, Oppenheimer J H

机构信息

Department of Medicine, University of Minnesota, Minneapolis 55455.

出版信息

Endocrinology. 1989 Dec;125(6):2868-74. doi: 10.1210/endo-125-6-2868.

Abstract

We have used the tritiated water method to quantitate the effects of thyroid hormone on lipogenesis in the rat and then determined the contribution of this process to thyroid hormone-induced thermogenesis. After thyroid hormone administration to hypothyroid animals, fatty acid synthesis rose after a lag time of 12-16 h and reached a plateau after 4-5 days. This is consistent with the kinetics of an increase in oxygen consumption measured by others in similar animals. A diurnal variation was maintained in all thyroid states, with the peak value in the middle of the dark period being 3-fold higher than the nadir. Fatty acid synthesis in the livers of hyperthyroid animals was 3- to 4-fold higher than that in euthyroid rats, which, in turn, was 3- to 5-fold higher than the rate observed in hypothyroid rats. Slightly smaller but similar fold increases were measured in epididymal fat. A stimulation of fatty acid synthesis by thyroid hormone was also measured in the rest of the carcass, with hyperthyroid rates being twice those in hypothyroid animals. The contribution of the liver was much greater in hyperthyroid rats (34% of total fatty acid synthesis) than in hypothyroid animals (5%). The energy costs of this synthesis were calculated and compared to published values for total oxygen consumption in different thyroid states. Thus, 6-10% of the total increment in oxygen consumption between hyperthyroid and hypothyroid animals could be attributed to lipogenesis, depending on which published figures were used. About 3% of this increment was due to the liver alone.

摘要

我们采用了氚水法来定量甲状腺激素对大鼠脂肪生成的影响,进而确定这一过程对甲状腺激素诱导的产热的贡献。给甲状腺功能减退的动物注射甲状腺激素后,脂肪酸合成在滞后12 - 16小时后上升,并在4 - 5天后达到平台期。这与其他研究人员在类似动物中测得的耗氧量增加的动力学一致。在所有甲状腺状态下均维持昼夜变化,黑暗期中期的峰值比最低点高3倍。甲状腺功能亢进动物肝脏中的脂肪酸合成比甲状腺功能正常的大鼠高3至4倍,而甲状腺功能正常的大鼠又比甲状腺功能减退的大鼠高3至5倍。在附睾脂肪中测得的增加倍数略小但相似。在胴体的其他部位也检测到甲状腺激素对脂肪酸合成的刺激,甲状腺功能亢进的速率是甲状腺功能减退动物的两倍。甲状腺功能亢进大鼠肝脏的贡献(占总脂肪酸合成的34%)比甲状腺功能减退动物(5%)大得多。计算了这种合成的能量成本,并与不同甲状腺状态下总耗氧量的已发表值进行了比较。因此,根据所使用的已发表数据,甲状腺功能亢进和甲状腺功能减退动物之间耗氧量总增加量的6 - 10%可归因于脂肪生成。仅肝脏就导致了这一增加量的约3%。

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