Durbin-Naltchayan S, Bouhnik J, Michel R
Horm Metab Res. 1983 Nov;15(11):547-9. doi: 10.1055/s-2007-1018784.
The thyroid function was explored by comparing serum total and free iodothyronine levels in young male genetically obese Zucker rats and in their lean littermates, aged from 6 to 8 weeks old. Total and free thyroxine (T4) and 3,5,3'triiodothyronine (T3) levels were significantly decreased in obese rat serum while total 3,3',5'-triiodothyronine (rT3) remained constant. Radioactive T4 half life is slower in the plasma of obese rats. Peripheral synthesis of T3 from deiodination of T4 is also decreased in obese rat liver homogenate. These modifications produce changes in liver mitochondria oxidative phosphorylation and in marker enzyme activity, which are usually associated with hypothyroidism and hypothalamic disturbances. Genetic obesity probably involves activation of peripheral deiodination of T4 to rT3 which induces biochemical and metabolic changes.
通过比较6至8周龄的年轻雄性遗传性肥胖 Zucker 大鼠及其瘦同胞的血清总甲状腺素和游离甲状腺素水平，对甲状腺功能进行了研究。肥胖大鼠血清中的总甲状腺素（T4）和游离甲状腺素以及3,5,3'-三碘甲状腺原氨酸（T3）水平显著降低，而总3,3',5'-三碘甲状腺原氨酸（反T3，rT3）保持不变。肥胖大鼠血浆中放射性T4的半衰期较慢。肥胖大鼠肝脏匀浆中由T4脱碘生成T3的外周合成也减少。这些变化导致肝脏线粒体氧化磷酸化和标记酶活性发生改变，这些改变通常与甲状腺功能减退和下丘脑功能紊乱有关。遗传性肥胖可能涉及T4外周脱碘生成rT3的激活，从而引起生化和代谢变化。
