Thyrotropin and prolactin responses to thyrotropin-releasing hormone: influence of fasting- and insulin-induced changes in glucose metabolism.
Thyrotropin and prolactin responses to thyrotropin-releasing hormone: influence of fasting- and insulin-induced changes in glucose metabolism.
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促甲状腺素和催乳素对促甲状腺素释放激素的反应：空腹和胰岛素诱导的葡萄糖代谢变化的影响。
DOI：
10.1016/0026-0495(83)90145-2
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
A. Nygren
中科院分区：
文献类型：
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作者：
S. Röjdmark;A. Nygren
据报道，长时间禁食可抑制正常人促甲状腺素（TSH）对促甲状腺素释放激素（TRH）的反应。为了探索TSH反应性降低背后的可能机制，并观察饮食因素是否影响催乳素（PRL）的反应，6名非肥胖志愿者在三个不同的禁食期后静脉注射小剂量的TRH (25 μg)：8小时过夜禁食，56小时禁食补充口服葡萄糖（4 g/kg/56 h，产生16千卡/kg/56 h）， 56小时禁食补充口服等量的含有17种不同氨基酸的氨基酸（AA）混合物（4 g/kg/56 h）。TRH使PRL水平从14±2 ng/ml提高到58±8 ng/ml。在两次延长禁食期后，获得了类似的PRL反应。禁食后，TRH使TSH水平由1.0±0.0 μU/ml提高到5.2±0.8 μU/ml。长时间禁食并补充葡萄糖对TSH反应性没有显著影响，也没有改变基础血糖水平。相比之下，延长禁食并补充AA不仅使TSH反应性降低了47±7% (P< 0.002)，还使基础血糖水平从4.2±0.1降至3.5±0.2 mmol/L （P< 0.002）。在另外6名禁食过夜的正常受试者中，分别在静脉注射胰岛素和静脉注射生理盐水后两次静脉注射25 μg TRH。胰岛素在30±3分钟内诱发市场低血糖（1.8±0.1 mmol/L），而生理盐水在相同时间内对血糖水平无显著影响。在胰岛素诱导的低血糖期间测量PRL反应性，发现PRL反应性提高了56±15% （P< 0.02）。相应的TSH反应性降低18±6% （P< 0.05）。这些结果表明，足够的葡萄糖输送到垂体促甲状腺激素可能是正常TSH反应的先决条件。他们还表明，葡萄糖利用的变化对乳养细胞和促甲状腺细胞的影响不同。
It has been reported that prolonged fasting inhibits the response of thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) in normal persons. To explore possible mechanisms behind this reduced TSH responsiveness and also to see whether dietary factors influence prolactin (PRL) responsiveness, six nonobese volunteers were intravenously injected with a small dose of TRH (25 μg) after three different fasting periods: an 8-hour overnight fast, a 56-hour fast supplemented with oral administration of glucose (4 g/kg/56 h yielding 16 kcal/kg/56 h), and a 56-hour fast supplemented with oral administration of an equicaloric amount of an amino acid (AA) mixture (4 g/kg/56 h) containing 17 different amino acids. The dose of TRH raised the PRL level from 14 ± 2 to 58 ± 8 ng/ml after the overnight fast. Similar PRL responses were obtained after the two prolonged fasting periods. The TRH also raised the TSH level from 1.0 ± 0.0 to 5.2 ± 0.8 μU/ml after the overnight fast. Prolonged fasting with glucose supplementation had no significant effect on this TSH responsiveness, nor did it change the basal blood glucose level. In contrast, prolonged fasting with AA supplementation not only reduced TSH responsiveness by 47 ± 7% (P< 0.002), it also lowered the basal blood glucose level from 4.2 ± 0.1 to 3.5 ± 0.2 mmol/L (P< 0.002). In an additional six normal subjects who fasted overnight, 25 μg TRH was injected intravenously on two occasions: after intravenous infusion of insulin, and after intravenous infusion of saline. The insulin induced market hypoglycemia (1.8 ± 0.1 mmol/L) in 30 ± 3 minutes, whereas saline, infused over a similar time period, had no significant influence on the blood glucose level. When PRL responsiveness was measured during the insulin-induced hypoglycemia, it was found to be increased by 56 ± 15% (P< 0.02). The corresponding TSH responsiveness was decreased by 18 ± 6% (P< 0.05). These results imply that an adequate glucose delivery to pituitary thyrotrophs might be a prerequisite for normal TSH responsiveness. They also show that changes in glucose utilization affect lactotrophs and thyrotrophs differently.