DeRuyter H, Burman K D, Wartofsky L, Smallridge R C
Horm Metab Res. 1984 Feb;16(2):92-6. doi: 10.1055/s-2007-1014705.
Previous studies have demonstrated that serum TSH and GH decrease during fasting. Taking advantage of the fact that somatostatin antiserum administration is an effective, specific method of blocking endogenous somatostatin activity, we performed the present investigation to explore whether known fasting-induced increases in somatostatin might underlie the mechanism(s) of this decrement. After a 48 hour fast, two groups of male rats were anesthetized and an indwelling right atrial catheter inserted. The control rats (n = 11) were injected with normal sheep serum and the experimental rats (n = 9) were injected with a specific antiserum to cyclic somatostatin; one and one-half hours later, blood was collected in a basal state after which 200 ng TRH was injected. The basal mean (+/- SE) T3 and T4 concentrations were 23 +/- 3 ng/dl and 1.9 +/- 0.1 ug/dl, respectively, in the fasted control group and 30 +/- 2 ng/dl and 2.3 +/- 0.2 ug/dl in the fasted somatostatin antiserum injected rats. While serum T4 and T3 levels were statistically unchanged between these two groups, basal TSH increased from 537 +/- 81 ng/ml in the control rats to 2913 +/- 742 ng/ml in the somatostatin antiserum-treated rats (P less than 0.05). Basal growth hormone levels were also higher in the somatostatin antiserum-injected rats (196 +/- 19 ng/ml vs 72 +/- 7 ng/ml (P less than 0.0025). TSH peak values following TRH injection were not different in the two study groups. In summary, the present study indicates that: (1) somatostatin antiserum increases both basal GH and TSH values in fasting rats; and (2) somatostatin and TRH may act through different pathways to modulate TSH secretion. By implication, therefore, it is suggested that enhanced somatostatin-like activity may represent one mechanism mediating the fasting-induced decrement observed in serum TSH and GH.
以往的研究表明，禁食期间血清促甲状腺激素（TSH）和生长激素（GH）会下降。利用注射生长抑素抗血清是一种有效、特异的阻断内源性生长抑素活性的方法这一事实，我们开展了本研究，以探究已知的禁食诱导的生长抑素增加是否可能是这种下降机制的基础。禁食48小时后，将两组雄性大鼠麻醉并插入右心房留置导管。对照组大鼠（n = 11）注射正常羊血清，实验组大鼠（n = 9）注射环状生长抑素特异性抗血清；1.5小时后，在基础状态下采集血液，之后注射200 ng促甲状腺激素释放激素（TRH）。禁食对照组大鼠基础状态下平均（±标准误）三碘甲状腺原氨酸（T3）和甲状腺素（T4）浓度分别为23±3 ng/dl和1.9±0.1 μg/dl，注射生长抑素抗血清的禁食大鼠中分别为30±2 ng/dl和2.3±0.2 μg/dl。虽然两组之间血清T4和T3水平在统计学上无变化，但基础TSH从对照组大鼠的537±81 ng/ml增加到生长抑素抗血清处理组大鼠的2913±742 ng/ml（P<0.05）。注射生长抑素抗血清的大鼠基础生长激素水平也更高（196±19 ng/ml对72±7 ng/ml，P<0.0025）。TRH注射后的TSH峰值在两个研究组中无差异。总之，本研究表明：（1）生长抑素抗血清可增加禁食大鼠的基础GH和TSH值；（2）生长抑素和TRH可能通过不同途径调节TSH分泌。因此，由此推断，生长抑素样活性增强可能是介导血清TSH和GH中观察到的禁食诱导下降的一种机制。
