Page M D, Koppeschaar H P, Edwards C A, Dieguez C, Scanlon M F
Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff.
Clin Endocrinol (Oxf). 1987 May;26(5):589-95. doi: 10.1111/j.1365-2265.1987.tb00814.x.
We have measured GH and PRL changes following separate and combined administration of insulin and GH releasing factor (GRF) in six normal males. Peak GH responses to separate administration of insulin and GRF were comparable (71.4 +/- 10.2 vs 70.1 +/- 27.7 mU/l; mean +/- SEM). However, the peak GH response following combined administration was significantly higher (120.8 +/- 29.7, P less than 0.05) as was the total GH released as calculated by measuring the area under the curve (P less than 0.05). In contrast the PRL response to hypoglycaemia was not altered by the combined administration of insulin and GRF. This effect was not due to any direct action of hypoglycaemia or insulin at pituitary level since basal and 10(-8) M GRF stimulated GH release from rat anterior pituitary cells in vitro was not influenced by varying glucose and insulin levels. Our findings support the hypothesis that GRF and insulin-induced hypoglycaemia release GH via different pathways which are, at least in part, additive.
我们测定了6名正常男性分别单独及联合给予胰岛素和生长激素释放因子(GRF)后生长激素(GH)和催乳素(PRL)的变化。单独给予胰岛素和GRF时,GH的峰值反应相当(分别为71.4±10.2与70.1±27.7 mU/l;均值±标准误)。然而,联合给药后的GH峰值反应显著更高(120.8±29.7,P<0.05),通过测量曲线下面积计算得出的总GH释放量也更高(P<0.05)。相比之下,联合给予胰岛素和GRF并未改变PRL对低血糖的反应。这种效应并非由于低血糖或胰岛素在垂体水平的任何直接作用,因为体外培养的大鼠垂体前叶细胞在基础状态及10(-8)M GRF刺激下的GH释放不受葡萄糖和胰岛素水平变化的影响。我们的研究结果支持以下假说:GRF和胰岛素诱导的低血糖通过不同途径释放GH,这些途径至少部分是相加的。