The effect of food deprivation of the peripheral metabolism of thyroxine in rats.
The effect of food deprivation of the peripheral metabolism of thyroxine in rats.
复制标题
食物剥夺对大鼠甲状腺素外周代谢的影响。
作者：
D. Ingbar;V. Galton
饥饿会抑制甲状腺功能。此外，甲状腺素（T4）的外周周转减少，部分原因是T4的粪便消除减少。本研究旨在确定饥饿是否也会影响T4降解的脱碘途径。每天注射外源性[131-I]T4使大鼠同位素平衡，同时用KCl 04阻断内源性甲状腺T4分泌和碘化物浓度。平衡一段时间后，对一半动物实施完全或50%的食物剥夺。在48小时的饥饿，血清T4浓度的完全饥饿的大鼠翻了一番，并始终保持高水平。T4粪便排泄量的显著减少是增加的部分原因。尽管尿131-I排泄量存在变异性，但放射性清除率始终降低。这些影响在恢复正常进食后很容易逆转。在半喂大鼠中观察到类似但不太严重的变化。在完全和部分饥饿的动物中，在血清T4水平升高的情况下，碘清除率降低表明外周脱碘作用受到某种未知机制的显著损害。与此相反，正常大鼠平衡剂量的T4足以增加血清T4水平表现出增加尿中清除碘来自T4。因此，血清T4水平升高是饥饿导致脱碘途径受损以及粪便T4排泄减少的结果。显然，在T4利用的实验研究期间，必须控制食物消耗的自愿改变以用于组间差异。
Starvation depresses thyroid gland function. In addition, the peripheral turnover of thyroxine (T4) is reduced, in part due to decreased fecal elimination of T4. The present studies were performed to determine if starvation also affects the deiodinative pathway for T4 degradation. Rats were isotopically equilibrated with daily injections of exogenous [131-I]T4 while endogenous thyroidal T4 secretion and concentration of iodide were blocked with KCl04. Following a period of equilibration, either complete or 50% food deprivation was imposed on half the animals. Within 48 h of starvation, the serum T4 concentration of the fully starved rats doubled and remained high throughout. A marked decrease in fecal excretion of T4 was partially responsible for the increase. In spite of variability in the quantity of urinary 131-I excreted, the dieodinative clearance was consistently reduced. These effects were readily reversible upon resumption of normal feeding. Similar though less severe changes were observed in the half-fed rats. In both fully and partially-starved animals, the decreased dieodinative clearance in the face of increased serum T4 levels indicates a significant impairment of peripheral deiodination by some as yet unknown mechanism. In contrast, normal rats equilibrated with doses of T4 sufficient to increase serum T4 levels exhibit increased urinary clearance of iodide derived from T4. Thus the increased serum T4 levels are a consequence of impairment of the deiodinative pathway by starvation as well as decreased fecal T4 excretion. Clearly, voluntary alterations in food consumption must be controlled for differences between groups during experimental studies of T4 utilization.