INVESTIGATION OF THE MECHANISM BY WHICH INSULIN-INDUCED HYPOGLYCEMIA DECREASES LUTEINIZING-HORMONE SECRETION IN OVARIECTOMIZED EWES
INVESTIGATION OF THE MECHANISM BY WHICH INSULIN-INDUCED HYPOGLYCEMIA DECREASES LUTEINIZING-HORMONE SECRETION IN OVARIECTOMIZED EWES
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DOI：
10.1210/endo-127-3-1470
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发表时间：
1990-09-01
期刊：
影响因子：
4.8
通讯作者：
DOUGHTON, BW
中科院分区：
文献类型：
--
作者：
CLARKE, IJ;HORTON, RJE;DOUGHTON, BW
卵巢切除母羊用100 IU胰岛素，静脉注射，导致血糖和血浆LH浓度降低。静脉注射葡萄糖可以阻止这种作用，这表明神经性低血糖症而不是胰岛素的直接作用是导致LH分泌减少的原因。在胰岛素注射前25分钟开始静脉输注纳洛酮（40 mg/h，持续2 h），可阻断胰岛素对LH分泌的抑制作用，但不能阻止血糖浓度的降低。在该治疗组和仅用纳洛酮治疗的组中，阿片拮抗剂显著刺激LH分泌。为了确定CRF是否可能参与胰岛素诱导的LH分泌减少，将50 μ g CRF注射到切除卵巢的绵羊中。尽管在注射后2分钟内产生非常高的CRF循环浓度，并且在治疗后4小时的大部分时间内刺激皮质醇分泌，但血浆LH水平未受影响。此外，脑室内施用10 μ g CRF或10 μ g CRF加10 μ g精氨酸加压素（AVP）不影响LH分泌。这些观察结果表明，胰岛素诱导的低血糖减少LH分泌的神经性低血糖症。这可能涉及阿片能机制，但不涉及下丘脑-垂体-肾上腺皮质轴的激活。
Ovariectomized ewes were treated with 100 IU insulin, iv, which caused reductions in blood sugar and plasma LH concentrations. The effect was prevented by the infusion (iv) of glucose, suggesting that neuroglycopenia and not a direct action of insulin was the cause of reduced LH secretion. An iv infusion of naloxone (40 mg/h for 2 h), which commenced 25 min before the insulin injection, blocked the inhibitory effect of insulin on LH secretion, but it did not prevent the decrease in plasma glucose concentrations. In this treatment group and in a group treated only with naloxone, the opioid antagonist significantly stimulted LH secretion. To determine whether CRF might be involved in the insulin-induced decrease in LH secretion, 50 .mu.g CRF were injected into ovariectomized sheep. Despite producing very high circulating concentrations of CRF within 2 min of injection and the stimulation of cortisol secretion during most of the 4-h posttreatment period, plasma LH levels were not affected. In addition, the intracerebroventricular administration of 10 .mu.g CRF or 10 .mu.g CRF plus 10 .mu.g arginine vasopressin (AVP) did not affect LH secretion. These observations suggest that insulin-induced hypoglycemia decreased LH secretion by neuroglycopenia. This may involve an opioidergic mechanism, but does not involve activation of the hypothalamo-pituitary-adrenocortical axis.