Burman K D, Smallridge R C, Osburne R, Dimond R C, Whorton N E, Kesler P, Wartofsky L
Metabolism. 1980 Jan;29(1):46-52. doi: 10.1016/0026-0495(80)90097-9.
TSH responses to 4-hr continuous TRH infusions of approximately 0.8 microgram/min were assessed during feeding (1500 Kcal), fasting, and refeeding (1500 Kcal) intervals in 9 euthyroid obese subjects. The total area under the TSH response curve was 1854 +/- 322 muU/ml . 4-hr during feeding, decreased to 1359 +/- 199 muU/ml . 4-hr (p less than 0.01) on the 10th day of fasting, and remained low, being 1405 +/- 185 muU/ml . 4-hr, despite refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) for 5 days. Baseline serum T3 concentrations were 167 +/- 11 ng/dl during feeding, 86 +/- 8 ng/dl during fasting, and 119 +/- 12 ng/dl during refeeding. The observed decreases in TSH release appeared to correlate with decreased biologic action on the thyroid gland since the net rise in T3 during the infusion was less in fasting and refeeding than in the control (fed) period. Basal serum rT3 levels were 42 +/- 5 ng/dl during feeding, rose as expected to 56 +/- 5 ng/dl during fasting (p less than 0.005), and were completely restored to normal during refeeding (36 +/- 5 ng/dl). These data suggest that: (1) TSH responsiveness to prolonged TRH infusion is diminished during fasting and does not return to control (fed) values despite 5 days of refeeding a 1500 Kcal diet; (2) net T3 increases observed during the TRH infusion are greater in the fed period than in the fasting or refeeding periods; and (3) 5 days of refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) did not return the T3 to its original fed value whereas rT3 was completely restored to control values. Lastly, since the TSH response was lower both during the early and late phases of the infusion, the decrease in delta TSH to a bolus of TRH during fasting appears to represent one manifestation of a more general suppression of TSH neogenesis associated with caloric deprivation.
在9名甲状腺功能正常的肥胖受试者的进食(1500千卡)、禁食和再进食(1500千卡)期间,评估了促甲状腺激素(TSH)对以约0.8微克/分钟的速度持续4小时静脉输注促甲状腺激素释放激素(TRH)的反应。TSH反应曲线下的总面积在进食期间为1854±322毫微单位/毫升·4小时,在禁食第10天时降至1359±199毫微单位/毫升·4小时(p<0.01),并且尽管再进食1500千卡饮食(40%碳水化合物、40%脂肪、20%蛋白质)5天,仍保持在较低水平,为1405±185毫微单位/毫升·4小时。进食期间的基础血清三碘甲状腺原氨酸(T3)浓度为167±11纳克/分升,禁食期间为86±8纳克/分升,再进食期间为119±12纳克/分升。观察到的TSH释放减少似乎与甲状腺的生物活性降低相关,因为输注期间T3的净增加量在禁食和再进食期间比对照(进食)期少。基础血清反三碘甲状腺原氨酸(rT3)水平在进食期间为42±5纳克/分升,如预期在禁食期间升至56±5纳克/分升(p<0.005),并在再进食期间完全恢复正常(36±5纳克/分升)。这些数据表明:(1)禁食期间TSH对延长的TRH输注的反应性降低,并且尽管再进食1500千卡饮食5天,仍未恢复到对照(进食)值;(2)TRH输注期间观察到的T3净增加量在进食期比禁食期或再进食期更大;(3)再进食1500千卡饮食(40%碳水化合物、40%脂肪、20%蛋白质)5天未使T3恢复到其原始进食值,而rT3完全恢复到对照值。最后,由于输注早期和晚期的TSH反应均较低,禁食期间TSH对TRH推注的变化量(ΔTSH)降低似乎代表了与热量剥夺相关的TSH新生普遍抑制的一种表现。