Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Endocrinology. 2009 Dec;150(12):5639-48. doi: 10.1210/en.2009-0297. Epub 2009 Oct 23.
The effects of thyroid hormone (TH) status on energy metabolism and tissue-specific substrate supply in vivo are incompletely understood. To study the effects of TH status on energy metabolism and tissue-specific fatty acid (FA) fluxes, we used metabolic cages as well as (14)C-labeled FA and (3)H-labeled triglyceride (TG) infusion in rats treated with methimazole and either 0 (hypothyroidism), 1.5 (euthyroidism), or 16.0 (thyrotoxicosis) microg per 100 g/d T(4) for 11 d. Thyrotoxicosis increased total energy expenditure by 38% (P = 0.02), resting energy expenditure by 61% (P = 0.002), and food intake by 18% (P = 0.004). Hypothyroidism tended to decrease total energy expenditure (10%; P = 0.064) and resting energy expenditure (12%; P = 0.025) but did not affect food intake. TH status did not affect spontaneous physical activity. Thyrotoxicosis increased fat oxidation (P = 0.006), whereas hypothyroidism decreased glucose oxidation (P = 0.035). Plasma FA concentration was increased in thyrotoxic but not hypothyroid rats. Thyrotoxicosis increased albumin-bound FA uptake in muscle and white adipose tissue (WAT), whereas hypothyroidism had no effect in any tissue studied, suggesting mass-driven albumin-bound FA uptake. During thyrotoxicosis, TG-derived FA uptake was increased in muscle and heart, unaffected in WAT, and decreased in brown adipose tissue. Conversely, during hypothyroidism TG-derived FA uptake was increased in WAT in association with increased lipoprotein lipase activity but unaffected in oxidative tissues and decreased in liver. In conclusion, TH status determines energy expenditure independently of spontaneous physical activity. The changes in whole-body lipid metabolism are accompanied by tissue-specific changes in TG-derived FA uptake in accordance with hyper- and hypometabolic states induced by thyrotoxicosis and hypothyroidism, respectively.
甲状腺激素（TH）状态对体内能量代谢和组织特异性底物供应的影响尚不完全清楚。为了研究 TH 状态对能量代谢和组织特异性脂肪酸（FA）通量的影响，我们使用代谢笼以及放射性标记的 FA 和放射性标记的三酰甘油（TG）输注，在甲状腺素处理的大鼠中使用甲巯咪唑，并且每天每 100 克体重给予 0（甲状腺功能减退）、1.5（甲状腺功能正常）或 16.0μg（甲状腺功能亢进）T4 11 天。甲状腺功能亢进症使总能量消耗增加 38%（P=0.02），静息能量消耗增加 61%（P=0.002），食物摄入增加 18%（P=0.004）。甲状腺功能减退症有使总能量消耗（减少 10%；P=0.064）和静息能量消耗（减少 12%；P=0.025）的趋势，但不影响食物摄入。TH 状态不影响自发体力活动。甲状腺功能亢进症增加脂肪氧化（P=0.006），而甲状腺功能减退症降低葡萄糖氧化（P=0.035）。血浆 FA 浓度在甲状腺功能亢进症大鼠中增加，但在甲状腺功能减退症大鼠中不增加。甲状腺功能亢进症增加肌肉和白色脂肪组织（WAT）中白蛋白结合的 FA 摄取，而甲状腺功能减退症在研究的任何组织中均无影响，表明 FA 摄取受质量驱动。在甲状腺功能亢进症期间，肌肉和心脏中 TG 衍生的 FA 摄取增加，WAT 中不受影响，棕色脂肪组织中减少。相反，在甲状腺功能减退症期间，WAT 中的 TG 衍生的 FA 摄取增加与脂蛋白脂肪酶活性增加有关，但在氧化组织中不受影响，在肝脏中减少。总之，TH 状态独立于自发体力活动决定能量消耗。整体脂质代谢的变化伴随着组织特异性 TG 衍生的 FA 摄取的变化，分别符合甲状腺功能亢进症和甲状腺功能减退症引起的高代谢和低代谢状态。
