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饮食对肥胖儿童胰岛素及胃抑肽水平的影响。

Effects of diet on insulin and gastric inhibitory polypeptide levels in obese children.

作者信息

Deschamps I, Heptner W, Desjeux J F, Baltakse V, Machinot S, Lestradet H

出版信息

Pediatr Res. 1980 Apr;14(4 Pt 1):300-3. doi: 10.1203/00006450-198004000-00008.

Abstract

To improve understanding of the relationships between gastric inhibitory polypeptide (GIP) and insulin secretion and food intake in obesity, immunoreactive insulin and immunoreactive GIP were measured in 5 obese children during PO glucose tolerance test carried out before and after diet. Before diet, mean insulin levels were normal at fasting and rose after glucose ingestion. The mean fasting immunoreactive GIP level was very high (1235 +- 209 pg/ml) compared to that of 8 healthy adult controls (411 +/- 44 pg/ml) and remained at this level throughout the test. There was only a short postabsorptive rise to 1515 +/- 158 pg/ml at 30 min, which was not significantly different either from the patients' basal values or from the 30-min control values (1356 +/- 67 pg/ml). After dieting for 3 to 7 months, immunoreactive insulin responses returned to normal ranges. Concomitantly, both basal and total GIP release diminished significantly (basal GIP, 343 +/- 92 pg/ml; area under the GIP curve, 3820 and 1694 pg/ml/hr before and after diet, respectively). The postabsorptive GIP increment, however, rose significantly from 180 pg/ml/hr, before diet, to 665 pg/ml/hr afterwards. These results might be compatible with the hypothesis that in obesity, hyperinsulinemia, and overactivity of the GIP cells are associated phenomena caused by overeating and reversed by reduced food intake. However, several contradictory findings remain unexplained. The discrepancy between insignificant postabsorptive GIP increments and elevated insulin responses before diet casts doubts on the causal relationship between GIP and insulin secretion. The small GIP rise might be due to a limited secretory capacity of the GIP cells or to a diminished stimulatory capacity of glucose. The constantly high level of GIP might reflect chronic hypersecretion and/or some defect in basal regulation and feedback control of GIP release. The change caused by dietary measures in the GIP secretion pattern provides evidence that in obese children, basal GIP secretion in influenced by nutritional factors.

摘要

为了更好地理解肥胖状态下胃抑制多肽(GIP)与胰岛素分泌及食物摄入之间的关系,我们对5名肥胖儿童在饮食前后进行口服葡萄糖耐量试验时测定了免疫反应性胰岛素和免疫反应性GIP。饮食前,空腹时胰岛素平均水平正常,摄入葡萄糖后升高。与8名健康成人对照组(411±44 pg/ml)相比,肥胖儿童空腹免疫反应性GIP平均水平非常高(1235±209 pg/ml),且在整个试验过程中维持在这一水平。仅在吸收后短时间内,30分钟时升至1515±158 pg/ml,这与患者的基础值或30分钟时的对照组值(1356±67 pg/ml)相比无显著差异。节食3至7个月后,免疫反应性胰岛素反应恢复到正常范围。同时,基础和总GIP释放均显著减少(基础GIP,343±92 pg/ml;饮食前后GIP曲线下面积分别为3820和1694 pg/ml/小时)。然而,吸收后GIP增量从饮食前的180 pg/ml/小时显著升至饮食后的665 pg/ml/小时。这些结果可能与以下假设相符:在肥胖状态下,高胰岛素血症和GIP细胞过度活跃是由暴饮暴食引起的相关现象,而减少食物摄入可使其逆转。然而,仍有一些相互矛盾的发现无法解释。饮食前吸收后GIP增量不显著与胰岛素反应升高之间的差异,让人对GIP与胰岛素分泌之间的因果关系产生怀疑。GIP的小幅升高可能是由于GIP细胞分泌能力有限或葡萄糖刺激能力降低。GIP持续高水平可能反映了慢性高分泌和/或GIP释放基础调节及反馈控制中的某些缺陷。饮食措施引起的GIP分泌模式变化提供了证据,表明在肥胖儿童中,基础GIP分泌受营养因素影响。

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