Obesity is associated with increased post-prandial GIP levels which are not reduced by dietary restriction and weight loss.

Obesity is associated with increased post-prandial GIP levels which are not reduced by dietary restriction and weight loss.
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肥胖与餐后 GIP 水平升高有关,而餐后 GIP 水平不会因饮食限制和体重减轻而降低。

DOI:
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发表时间:
1989
期刊:
Diabete & metabolisme
影响因子:
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通讯作者:
T. M. Hayes
T. M. Hayes
中科院分区:
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文献类型:
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作者:
I. Jones;D. Owens;S. Luzio;T. M. Hayes

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肥胖的特征是空腹和餐后高胰岛素血症。一个可能导致这种情况的因素是肠岛轴的过度活动。因此,在口服葡萄糖(OGTT)、混合餐(MTT)和静脉内葡萄糖耐量试验(IVGTT)期间,对瘦型(IBW小于120%)和肥胖型(IBW大于120%)健康受试者的葡萄糖耐量、β细胞反应和GIP谱进行了比较。在饮食限制和体重减轻一段时间后,肥胖组重复了这些测试。空腹GIP浓度相似,但在OGTT和MTT期间,肥胖受试者的餐后水平显著更高。血糖曲线相似,但与肥胖受试者的基础和刺激高胰岛素血症相关,表明胰岛素抵抗。在IVGTT期间,GIP水平没有变化,并且在整个测试期间两组中相似。节食和减肥后,肥胖受试者的空腹和餐后胰岛素水平显著降低,但葡萄糖或GIP浓度没有显著变化。总之,内源性刺激的血浆GIP反应在肥胖健康受试者中被夸大,但这种增加的反应不会因短期饮食和体重减轻而降低。GIP浓度增加可能导致肥胖症中观察到的高胰岛素血症,但鉴于饮食和体重减轻后胰岛素浓度降低(与GIP的任何变化无关),其贡献可能很小。
Obesity is characterised by fasting and post-prandial hyperinsulinaemia. One factor which may contribute to this is overactivity of the enteroinsular axis. Glucose tolerance, beta-cell response and GIP profiles were therefore compared during oral glucose (OGTT), mixed meal (MTT) and intravenous glucose tolerance tests (IVGTT) in both lean (IBW less than 120%) and obese (IBW greater than 120%) healthy subjects. The tests were repeated in the obese group after a period of dietary restriction and weight loss. Fasting GIP concentrations were similar, but postprandial levels were significantly greater in the obese subjects during both the OGTT and MTT. Glucose profiles were similar but associated with basal and stimulated hyperinsulinaemia in the obese subjects indicating insulin resistance. GIP levels did not change during the IVGTT and were similar in the two groups throughout the test. Following diet and weight-reduction there was a significant decrease in both fasting and post-prandial insulin levels in the obese subjects but there were no significant changes in glucose or GIP concentrations. In conclusion the endogenously stimulated plasma GIP response is exaggerated in obese healthy subjects but this increased response is not decreased by short term diet and weight loss. The increased GIP concentrations may contribute the observed hyperinsulinaemia in obesity, but its contribution is likely to be small in view of the decrease in insulin concentrations following diet and weight-loss which was independent of any change in GIP.