DeCherney G S, DeBold C R, Jackson R V, Sheldon W R, Kamilaris T C, Island D P, Orth D N
J Clin Endocrinol Metab. 1987 Jun;64(6):1211-8. doi: 10.1210/jcem-64-6-1211.
The factors that mediate the hypothalamic-pituitary response to hypoglycemia in man are unknown. To investigate the role of CRH in the plasma ACTH response to hypoglycemia, two different doses of ovine CRH (oCRH) were given to normal men during insulin-induced hypoglycemia. We hypothesized that if the endogenous CRH response to hypoglycemia were less than maximally stimulating, administration of oCRH during hypoglycemia would result in a greater peak plasma immunoreactive (IR) ACTH response. Six normal men were given 1) 0.15 U/kg regular insulin, iv; 2) insulin plus 1 microgram/kg oCRH, iv, 5 min after serum glucose fell to 40 mg/dL or less; and 3) oCRH alone. The degree and duration of hypoglycemia were the same when insulin was given alone or with oCRH. Plasma IR-ACTH after insulin alone and insulin plus oCRH rose at the same rate to similar peaks of 226 +/- 37 (mean +/- SEM) and 213 +/- 53 pg/mL, respectively, both of which were greater (P less than 0.05) than the peak plasma IR-ACTH after oCRH alone (61 +/- 19 pg/mL). The peak plasma IR-cortisol levels after insulin alone (24 +/- 4 micrograms/dL), insulin plus oCRH (27 +/- 3 micrograms/dL), and oCRH alone (18 +/- 2 micrograms/dL) were not significantly different. In a second study, six normal men were given 0.15 U/kg regular insulin, iv; insulin plus 10 micrograms/kg oCRH, iv; and 10 micrograms/kg oCRH alone. Administration of oCRH 5 min after serum glucose fell to 40 mg/dL or less did not affect the degree or duration of hypoglycemia. Plasma IR-ACTH after insulin alone and insulin plus oCRH rose at the same rate to similar peaks of 258 +/- 14 and 290 +/- 33 pg/mL, respectively, both of which were greater (P less than 0.01) than the peak (54 +/- 6 pg/mL) after oCRH alone. After insulin alone, plasma IR-ACTH declined to baseline by 3 h. However, after insulin plus oCRH, plasma IR-ACTH fell gradually until 2 h, rose to a second peak at 2.5-3 h, and remained greater (P less than 0.01) than after insulin or oCRH alone for the 4-h duration of the study. The mean peak plasma IR-cortisol level after insulin plus oCRH (33 +/- 4 micrograms/dL) was similar to that after insulin alone (28 +/- 3 micrograms/dL), but was greater (P less than 0.05) than that after oCRH alone (18 +/- 2 micrograms/dL).(ABSTRACT TRUNCATED AT 400 WORDS)
介导人体下丘脑 - 垂体对低血糖反应的因素尚不清楚。为了研究促肾上腺皮质激素释放激素（CRH）在血浆促肾上腺皮质激素（ACTH）对低血糖反应中的作用，在胰岛素诱导的低血糖期间，给正常男性注射两种不同剂量的羊CRH（oCRH）。我们假设，如果内源性CRH对低血糖的反应未达到最大刺激程度，那么在低血糖期间给予oCRH将导致血浆免疫反应性（IR）ACTH反应峰值更高。六名正常男性分别接受：1）静脉注射0.15 U/kg正规胰岛素；2）在血糖降至40 mg/dL或更低后5分钟，静脉注射胰岛素加1 μg/kg oCRH；3）单独注射oCRH。单独给予胰岛素或与oCRH一起给予时，低血糖的程度和持续时间相同。单独注射胰岛素和胰岛素加oCRH后，血浆IR-ACTH以相同速率上升至相似峰值，分别为226±37（平均值±标准误）和213±53 pg/mL，两者均高于单独注射oCRH后的血浆IR-ACTH峰值（61±19 pg/mL，P<0.05）。单独注射胰岛素（24±4 μg/dL）、胰岛素加oCRH（27±3 μg/dL）和单独注射oCRH（18±2 μg/dL）后的血浆IR-皮质醇峰值无显著差异。在第二项研究中，六名正常男性接受：静脉注射0.15 U/kg正规胰岛素；静脉注射胰岛素加10 μg/kg oCRH；单独注射10 μg/kg oCRH。在血糖降至40 mg/dL或更低后5分钟给予oCRH，不影响低血糖的程度或持续时间。单独注射胰岛素和胰岛素加oCRH后，血浆IR-ACTH以相同速率上升至相似峰值，分别为258±14和290±33 pg/mL，两者均高于单独注射oCRH后的峰值（54±6 pg/mL，P<0.01）。单独注射胰岛素后，血浆IR-ACTH在3小时内降至基线。然而，胰岛素加oCRH后，血浆IR-ACTH在2小时内逐渐下降，在2.5 - 3小时升至第二个峰值，并在研究的4小时内一直高于单独注射胰岛素或oCRH后的水平（P<0.01）。胰岛素加oCRH后的平均血浆IR-皮质醇峰值水平（33±4 μg/dL）与单独注射胰岛素后的水平（28±3 μg/dL）相似，但高于单独注射oCRH后的水平（18±2 μg/dL，P<0.05）。（摘要截取自400字）
