Characteristics of thyroid function in experimental protein malnutrition.
Characteristics of thyroid function in experimental protein malnutrition.
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实验性蛋白质营养不良的甲状腺功能特征。
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
E. Horton
中科院分区：
文献类型：
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作者：
O. Tulp;P. Krupp;E. Danforth;E. Horton
本文通过两个实验研究了蛋白质营养不良对甲状腺功能的影响。在断奶后28或32天，雄性大鼠随意喂食含22%（对照）或8%（蛋白质营养不良，PM）酪蛋白的等能饲料，测定其静息耗氧量和血清三碘甲状腺原氨酸（T3）、甲状腺素（T4）和促甲状腺激素（TSH）浓度，并与甲状腺组织学、增重、饲料效率和胴体能量含量相关。第三组用对照饮食配对喂养PM大鼠。在实验2中，另外的组用8%酪蛋白饮食对喂PM大鼠，其中酪蛋白被不同的碳水化合物和脂肪的混合物替代。在所有组中，静息耗氧量/体重（0.75）随体重增加而降低，但在PM大鼠中始终最大。在PM大鼠中，11天的饮食方案后，血浆T3为对照组的130%，从第18天到第32天平均为对照组的215%。在实验2中，所有PM组中T3和T4浓度均约为对照组的两倍。所有组的TSH浓度始终在正常范围内。饲料效率平均为对照组的36%至40%，PM组28天后的平均体重增加为30 g，而配对喂养的对照大鼠分别为114 g和91 g。28天后PM大鼠的胴体能量含量显着低于对照组或配对喂养的对照组大鼠。甲状腺形态与所有蛋白质营养不良组的分泌活动增加相一致，而对照组和配对喂养对照组的分泌活动正常。产热，测量的耗氧量，显着增加PM大鼠相比，控制。这些观察结果与蛋白质营养不良大鼠的饮食诱导产热一致。与单纯的营养不良（其中能量消耗可以通过甲状腺功能和产热作用的降低来保存）相反，蛋白质营养不良中甲状腺功能和产热作用的增加可以提供能量平衡机制，由此饮食中不需要的非蛋白质能量可以作为热量消散，并且存活率提高。
Two experiments were conducted to study the effects of protein malnutrition on thyroid function. Resting oxygen consumption and serum concentrations of triiodothyronine (T3), thyroxine (T4) and thyroid stimulating hormone (TSH) were measured and correlated with thyroid histology, gain in weight, feed efficiency and carcass energy content in male rats fed isoenergetic diets ad libitum containing 22% (control) or 8% (protein malnourished, PM) casein for 28 or 32 days postweaning. A third group was pair-fed to the PM rats with the control diet. In experiment 2 additional groups were pair-fed to the PM rats with 8% casein diets in which the casein was substituted with different mixtures of carbohydrate and fat. Resting oxygen consumption/body weight (0.75) decreased as body weights increased in all groups, but was consistently greatest in PM rats. In PM rats, plasma T3 was 130% of controls after 11 days of the dietary regimen and averaged 215% of controls from days 18 through 32. In experiment 2 both T3 and T4 concentrations were approximately twice controls in all PM groups. TSH concentrations were within the normal range in all groups throughout. Feed efficiency averaged 36 to 40% of controls and mean weight gain was 30 g after 28 days in the PM groups, compared to 114 and 91 g, respectively, in the pair-fed control rats. Carcass energy content of PM rats after 28 days was significantly lower than in control or pair-fed control rats. Thyroid morphology was compatible with increased secretory activity in all the protein-malnourished groups, compared with normal activity in the control and pair-fed control groups. Thermogenesis, as measured by oxygen consumption, was markedly increased in the PM rats compared to controls. These observations are consistent with a diet-induced thermogenesis in the protein-malnourished rats. In contrast to simple under-nutrition where energy expenditure may be conserved by decreases in thyroid function and thermogenesis, increases in thyroid function and thermogenesis in protein malnutrition could provide an energy balancing mechanism whereby unneeded non-protein energy in the diet could be dissipated as heat, and survival enhanced.