Janowski B A, Ling N C, Giustina A, Wehrenberg W B
Dept. of Health Sciences, University of Wisconsin-Milwaukee 53211.
Life Sci. 1993;52(11):981-7. doi: 10.1016/0024-3205(93)90534-a.
Suppressed pulsatile GH secretion in food-deprived rats has been hypothesized to be due to an increase in hypothalamic somatostatin secretion. We investigated this hypothesis and the role of GHRH in regulating GH secretion during food deprivation using two different models. In experiment one, rats were food deprived for 72h during which time they received a saline infusion (n = 5). At the same time rats were normal fed for 72h during which time they received a somatostatin infusion (5 micrograms/h, n = 7). After the 72h infusion period, all rats received two iv injections of GHRH (1 microgram/rat) at 2h intervals. GH concentrations in food-deprived rats rose from approximately 10 ng/ml to 400-800 ng/ml in response to both GHRH injections. This increase was significantly greater (p < 0.01) than the GH response (100-400 ng/ml) observed in somatostatin-infused animals. The significantly higher GH response observed in food-deprived rats as compared to somatostatin-infused, normal-fed rats suggests that somatostatin concentrations may decrease during food deprivation. In experiment two, rats were infused for 5h with either saline (n = 6) or GHRH (10 micrograms/h, n = 9) at the end of a 72h fast. GH concentrations did not change in saline-infused animals. In contrast, GH concentrations significantly increased (p < 0.01) upon initiation of the continuous GHRH infusion. Yet, this release of GH was pulsatile in nature. Pulsatile GH secretion in the presence of a constant GHRH infusion suggests that pulsatile somatostatin release from the hypothalamus is maintained during food deprivation. These studies suggest that during food deprivation in the rat 1) absolute concentrations of somatostatin decrease, but its pattern of secretion remains pulsatile, and 2) decreased GHRH release may be responsible for the absence of spontaneous GH pulses.
食物缺乏的大鼠中脉冲式生长激素（GH）分泌受抑制，据推测这是由于下丘脑生长抑素分泌增加所致。我们使用两种不同模型研究了这一假说以及生长激素释放激素（GHRH）在食物缺乏期间调节GH分泌中的作用。在实验一中，大鼠食物缺乏72小时，在此期间给予生理盐水输注（n = 5）。同时，大鼠正常进食72小时，在此期间给予生长抑素输注（5微克/小时，n = 7）。在72小时输注期结束后，所有大鼠每隔2小时静脉注射两次GHRH（1微克/只）。食物缺乏的大鼠在两次GHRH注射后，GH浓度从约10纳克/毫升升至400 - 800纳克/毫升。这一增加显著大于（p < 0.01）生长抑素输注动物中观察到的GH反应（100 - 400纳克/毫升）。与生长抑素输注、正常进食的大鼠相比，食物缺乏的大鼠中观察到的显著更高的GH反应表明，食物缺乏期间生长抑素浓度可能降低。在实验二中，大鼠在禁食72小时结束时，用生理盐水（n = 6）或GHRH（10微克/小时，n = 9）输注5小时。生理盐水输注的动物中GH浓度未变化。相反，持续输注GHRH后，GH浓度显著增加（p < 0.01）。然而，这种GH释放本质上是脉冲式的。在持续输注GHRH的情况下出现脉冲式GH分泌表明，食物缺乏期间下丘脑脉冲式生长抑素释放得以维持。这些研究表明，在大鼠食物缺乏期间：1）生长抑素的绝对浓度降低，但其分泌模式仍为脉冲式；2）GHRH释放减少可能是自发GH脉冲缺失的原因。
