Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity
Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity
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DOI：
10.1530/eje.0.1350205
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发表时间：
1996-08-01
影响因子：
5.8
通讯作者：
Ghigo, E
中科院分区：
文献类型：
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作者：
Maccario, M;Grottoli, S;Ghigo, E
在高催乳素血症患者中，有报告称葡萄糖诱导的胰岛素分泌过度，但这些结果尚未得到其他研究人员的证实。另一方面，关于这种情况下生长激素分泌的数据很少，为了阐明这些观点，在7名正常体重的高催乳素血症女性患者中，（HP：年龄18-46岁，体重指数= 21.8 +/- 0.6 kg/m（2），基础催乳素= 91.7 +/- 16.5 μ g/l），我们研究了葡萄糖负荷（口服100 g）和/或精氨酸（30分钟内输注0.5 g/kg）对胰岛素葡萄糖和生长激素（GH）水平的影响。这些结果与7例单纯性肥胖患者（OB：年龄23-48岁，体重指数= 38.3 +/- 2.6 kg/m2）的结果进行了比较，这些患者的胰岛素分泌过多和GH分泌不足是众所周知的。7名正常女性（NS：年龄26-32岁，体重指数= 20.6 +/- 1.9 kg/m2）作为对照。min . 1（-1））与NS（7743.7 +/- 882.9 mU）无显著差异。min . 1（-1））和OB（14504.8 ± 1659.9 mU . min . 1（-1））。在HP和OB中，精氨酸诱导的胰岛素释放相似（4219.4 +/- 631.7和4107.3 +/- 643.2 mU。min . 1（-1）），两者均高于（p < 0.02）NS（2178.1 +/-290.9 mU . min . 1（-1））。葡萄糖和精氨酸对HP和NS中的胰岛素释放具有累加效应（19769.1 +/- 3249.6和10996.6 +/- 1201.0 mU）。min . 1（-1））和OB中的协同效应（28117.3 +/- 5224.7 mU . min . 1（-1））。HP组与OB组胰岛素对葡萄糖和精氨酸联合给药的反应无显著性差异，但均高于NS组（p < 0.05）。OB组单独或联合给药后葡萄糖水平的升高高于NS组和HP组（p < 0.02），且持续时间较长。在OB中加入精氨酸后，葡萄糖水平并没有表现出KP和NS中观察到的低于基线值的晚期下降。葡萄糖抑制HP和NS中的GH分泌（p < 0.05），而精氨酸在所有组中刺激GH分泌，尽管KP和NS中的GH反应高于OB（p < 0.03）。葡萄糖对HP和NS的GH分泌有抑制作用，但对OB无抑制作用。这些结果表明，在高催乳素血症患者和肥胖患者中，胰岛素分泌明显增加。高催乳素血症中的胰岛素高反应性通过葡萄糖和精氨酸的联合刺激更清楚地证明。尽管高催乳素血症和肥胖患者的胰岛素分泌过多相似，但仅后者的GH分泌减少;根据这些数据，肥胖患者的生长激素不足是由于高胰岛素血症的假设不太可能。
In hyperprolactinemic patients an exaggerated glucose-induced insulin secretion has been reported, but these results have not been confirmed by other researchers. On the other hand, there are few data concerning somatotrope secretion in this condition, In order to clarify these points, in seven normal weight hyperprolactinemic female patients (HP: age 18-46 years, body mass index = 21.8 +/- 0.6 kg/m(2), basal prolactin = 91.7 +/- 16.5 mu g/l) we studied the effects of glucose load (100 g orally) and/or arginine (0.5 g/kg infused over 30 min) on insulin glucose and growth hormone (GH) levels. These results were compared with those obtained in seven patients with simple obesity (OB: age 23-48 years, body mass index = 38.3 +/- 2.6 kg/m(2)) in whom exaggerated insulin and low GH secretion are well known. Seven normal women (NS: age 26-32 years, body mass index = 20.6 +/- 1.9 kg/m(2)) were studied as controls, The insulin response to glucose in HP (area under curve = 11460.8 +/- 1407.5 mU . min . 1(-1)) was not significantly different from NS (7743.7 +/- 882.9 mU . min . 1(-1)) and OB (14504.8 +/- 1659.9 mU . min . 1(-1)). The arginine-induced insulin release in HP and OB was similar (4219.4 +/- 631.7 and 4107.3 +/- 643.2 mU . min . 1(-1), respectively), both being higher (p < 0.02) than in NS (2178.1 +/- 290.9 mU . min . 1(-1)). Glucose and arginine had an additive effect on insulin release in HP and NS (19769.1 +/- 3249.6 and 10996.6 +/- 1201.0 mU . min . 1(-1), respectively) and a synergistic effect in OB (28117.3 +/- 5224.7 mU . min . 1(-1)). In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS, The increase in glucose levels after glucose administered on its own or combined with arginine was higher (p < 0.02) and longer lasting in OB than in NS and HP. After arginine in OB, the glucose levels did not show the late decrease under baseline values observed in KP and NS, Glucose inhibited GH secretion both in HP and NS (p < 0.05), while arginine stimulated it in all groups, although the GH response in KP and NS was higher (p < 0.03) than in OB. The arginine-induced GH secretion was inhibited by glucose in HP and NS but not in OB. These results demonstrate that both in hyperprolactinemic patients and in obesity there is a clear increase in insulin secretion, The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. In spite of similar insulin hypersecretion in hyperprolactinemic and obese patients, GH secretion is reduced only in the latter; with these data the hypothesis that somatotrope insufficiency in obesity is due to hyperinsulinism is unlikely.