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血浆葡萄糖依赖型胰岛素多肽水平升高与代谢综合征中的高胰岛素血症有关。

Elevated plasma glucose-dependent insulinotropic polypeptide associates with hyperinsulinemia in metabolic syndrome.

机构信息

Department of Clinical and Molecular Biomedicine, University of Catania, Ospedale Garibaldi Nesima, Via Palermo 636, 95122 Catania, Italy.

出版信息

Eur J Endocrinol. 2012 May;166(5):917-22. doi: 10.1530/EJE-11-0765. Epub 2012 Mar 5.

DOI:10.1530/EJE-11-0765
PMID:22391044
Abstract

BACKGROUND AND AIMS

Metabolic syndrome (MS) is a high-risk condition for type 2 diabetes, a disease characterized by insulin resistance and insulin secretion abnormalities. Insulin resistance has been widely characterized in MS subjects while insulin secretion has been poorly investigated. The present study was hence undertaken to further investigate the α and β cell function and entero-insular axis in this pre-diabetic condition.

MATERIALS AND METHODS

Using 120' oral glucose tolerance test (OGTT, 75  g) and 60' intravenous glucose tolerance test (IVGTT, 0.3  g/kg), we studied α and β cell function, insulin resistance, and incretin levels in 96 subjects with normal fasting glucose and normal glucose tolerance to OGTT, with (MS+, n=29) and without MS (MS-, n=67).

RESULTS

MS+ individuals showed in comparison with MS-: higher insulinogenic index (IG30) and higher area under the curve (AUC) (0-120) for glucose and insulin during the OGTT, P<0.05; higher AUC (0-10) for glucose (P<0.05) but similar first phase insulin secretion (P=NS) as measured by ΔAIRG and AUC (0-10) for insulin during the IVGTT; increased AUC (0-60) for insulin during the IVGTT (P=0.04); higher GIP levels at 30' (P=0.03), 60' (P=0.01), 90' (P=0.003), and 120' (P=0.004); higher AUC (0-120) for GIP (P=0.007); similar AUC (0-120) for GLP-1 during the OGTT; and delayed glucagon suppression after the OGTT.

CONCLUSION

NGT subjects with MS showed increased GIP secretion that could be responsible for the delayed glucagon suppression during the OGTT, thereby suggesting a role for incretins in regulating glucose homeostasis in this condition.

摘要

背景与目的

代谢综合征(MS)是 2 型糖尿病的高危状态,2 型糖尿病的特征为胰岛素抵抗和胰岛素分泌异常。胰岛素抵抗在 MS 患者中已得到广泛研究,而胰岛素分泌则研究不足。因此,本研究旨在进一步研究这种糖尿病前期状态下的α和β细胞功能以及肠胰岛轴。

材料与方法

我们使用 120 分钟口服葡萄糖耐量试验(OGTT,75g)和 60 分钟静脉葡萄糖耐量试验(IVGTT,0.3g/kg),研究了 96 例空腹血糖和 OGTT 正常的受试者的α和β细胞功能、胰岛素抵抗和肠促胰岛素水平,其中 29 例(MS+)和 67 例(MS-)存在 MS。

结果

与 MS-相比,MS+个体在 OGTT 中表现出更高的胰岛素原指数(IG30)和葡萄糖及胰岛素的曲线下面积(AUC)(0-120),P<0.05;在 OGTT 中葡萄糖的 AUC(0-10)更高(P<0.05),但 IVGTT 中第一时相胰岛素分泌的 AUC(0-10)和胰岛素相似(P=NS);IVGTT 中胰岛素的 AUC(0-60)更高(P=0.04);30'(P=0.03)、60'(P=0.01)、90'(P=0.003)和 120'(P=0.004)时 GIP 水平更高;GIP 的 AUC(0-120)更高(P=0.007);OGTT 期间 GLP-1 的 AUC(0-120)相似;OGTT 后胰高血糖素抑制延迟。

结论

存在 MS 的 NGT 受试者表现出 GIP 分泌增加,这可能是 OGTT 期间胰高血糖素抑制延迟的原因,表明肠促胰岛素在这种情况下对葡萄糖稳态的调节作用。

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