Basu Ananda, Dalla Man Chiara, Basu Rita, Toffolo Gianna, Cobelli Claudio, Rizza Robert A
Division of Endocrinology and Metabolism, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Diabetes Care. 2009 May;32(5):866-72. doi: 10.2337/dc08-1826. Epub 2009 Feb 5.
In this study, we sought to determine whether postprandial insulin secretion, insulin action, glucose effectiveness, and glucose turnover were abnormal in type 2 diabetes.
Fourteen subjects with type 2 diabetes and 11 nondiabetic subjects matched for age, weight, and BMI underwent a mixed-meal test using the triple-tracer technique. Indexes of insulin secretion, insulin action, and glucose effectiveness were assessed using the oral "minimal" and C-peptide models.
Fasting and postprandial glucose concentrations were higher in the diabetic than nondiabetic subjects. Although peak insulin secretion was delayed (P < 0.001) and lower (P < 0.05) in type 2 diabetes, the integrated total postprandial insulin response did not differ between groups. Insulin action, insulin secretion, disposition indexes, and glucose effectiveness all were lower (P < 0.05) in diabetic than in nondiabetic subjects. Whereas the rate of meal glucose appearance did not differ between groups, the percent suppression of endogenous glucose production (EGP) was slightly delayed and the increment in glucose disappearance was substantially lower (P < 0.01) in diabetic subjects during the first 3 h after meal ingestion. Together, these defects resulted in an excessive rise in postprandial glucose concentrations in the diabetic subjects.
When measured using methods that avoid non-steady-state error, the rate of appearance of ingested glucose was normal and suppression of EGP was only minimally impaired. However, when considered in light of the prevailing glucose concentration, both were abnormal. In contrast, rates of postprandial glucose disappearance were substantially decreased due to defects in insulin secretion, insulin action, and glucose effectiveness.
在本研究中,我们试图确定2型糖尿病患者的餐后胰岛素分泌、胰岛素作用、葡萄糖效能及葡萄糖周转率是否异常。
14名2型糖尿病患者和11名年龄、体重及体重指数相匹配的非糖尿病受试者采用三重示踪技术进行混合餐试验。使用口服“最小量”和C肽模型评估胰岛素分泌、胰岛素作用及葡萄糖效能指标。
糖尿病患者空腹及餐后血糖浓度高于非糖尿病受试者。虽然2型糖尿病患者的胰岛素分泌峰值延迟(P<0.001)且较低(P<0.05),但餐后胰岛素反应的综合总量在两组间并无差异。糖尿病患者的胰岛素作用、胰岛素分泌、处置指数及葡萄糖效能均低于非糖尿病受试者(P<0.05)。尽管两组间餐时葡萄糖出现率无差异,但糖尿病患者在摄入餐后的前3小时内,内源性葡萄糖生成(EGP)的抑制百分比略有延迟,且葡萄糖消失的增加量显著降低(P<0.01)。这些缺陷共同导致糖尿病患者餐后血糖浓度过度升高。
当采用避免非稳态误差的方法测量时,摄入葡萄糖的出现率正常,EGP的抑制仅轻微受损。然而,鉴于当时的血糖浓度,两者均异常。相比之下,由于胰岛素分泌、胰岛素作用及葡萄糖效能的缺陷,餐后葡萄糖消失率大幅降低。