Are fasting-induced effects on thyrotropin and prolactin secretion mediated by dopamine?
Are fasting-induced effects on thyrotropin and prolactin secretion mediated by dopamine?
复制标题
禁食对促甲状腺素和催乳素分泌的影响是由多巴胺介导的吗？
DOI：
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发表时间：
1983
影响因子：
5.8
通讯作者：
S. Röjdmark
中科院分区：
文献类型：
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作者：
S. Röjdmark
为了研究总热量剥夺是否会影响TSH和/或PRL的反应性，7名健康志愿者禁食过夜（8小时），静脉注射小剂量（25微克）的TRH和30分钟后40毫克西咪替丁（CIM）。在禁食56小时后，在相同的个体中重复TRH-CIM联合试验。TRH刺激的平均最大TSH增量在禁食期间从5.1 +/- 1.2降至1.2 +/- 0.6 microU/ml（P <0.01）。相反，TRH和CIM诱导的PRL反应均不受影响。为了排除TSH反应性降低的方法学错误，另外4名正常受试者禁食56小时，然后单独给予TRH。两天后，TRH试验在仅禁食8小时后重复。这个实验设计也导致了一个显着较低的TSH反应后较长的禁食期比后较短的时间，从而表明，无论饥饿期之前或之后的TRH注射，无论是否与TRH加CIM刺激垂体促甲状腺激素细胞，或与TRH单独延长禁食抑制TSH反应。在另外7名健康受试者注射TRH加CIM之前和之后禁食56小时，多巴胺D-2受体阻断剂，甲氧氯普胺（MET），口服90分钟前第二TRH-CIM负荷。MET的这种引发未能恢复禁食受试者的正常TSH反应性，因此表明抑制的TSH分泌不可能通过多巴胺D-2受体介导。然而，由于口服MET预处理完全取消了CIM引起的PRL反应，在空腹受试者，这是合理的假设，CIM刺激PRL释放通过减少多巴胺能抑制垂体催乳素。
To investigate whether total caloric deprivation influences TSH and/or PRL responsiveness, seven healthy volunteers fasted overnight (8 h) and were injected iv with a small dose (25 micrograms) of TRH and 30 min later with 40 mg cimetidine (CIM). This combined TRH-CIM test was repeated in the same individuals after a fasting period of 56 h. The TRH-stimulated mean maximal TSH increment fell from 5.1 +/- 1.2 to 1.2 +/- 0.6 microU/ml (P less than 0.01) during fasting. In contrast, both the TRH- and CIM-induced PRL responses were unaffected. To exclude methodologic errors on this reduced TSH responsiveness, an additional four normal subjects fasted for 56 h and then were given TRH alone. Two days later the TRH test was repeated after a fasting period of only 8 h. This experimental design also resulted in a significantly lower TSH response after the longer fasting period than after the shorter period, thus demonstrating that prolonged fasting inhibits TSH responsiveness regardless of whether the starvation period precedes or follows the TRH injection, and regardless of whether the pituitary thyrotrophs are stimulated with TRH plus CIM, or with TRH alone. In an additional seven healthy subjects injected with TRH plus CIM before and after a fasting period of 56 h, a dopamine D-2 receptor blocking agent, metoclopramide (MET), was given orally 90 min before the second TRH-CIM load. This priming with MET failed to restore normal TSH responsiveness in the fasting subjects, thus indicating that the suppressed TSH secretion could not have been mediated through dopamine D-2 receptors. However, since oral pretreatment with MET completely abolished the CIM-elicited PRL response in the fasting subjects, it is reasonable to assume that CIM stimulates PRL release via a reduced dopaminergic inhibition of the pituitary lactotrophs.