Abdul-Ghani Muhammad A, Williams Ken, DeFronzo Ralph, Stern Michael
Diabetes Division, University of Texas Health Science Center, 7703 Floyd Curl Dr., MS 7886, San Antonio, 78229, USA.
Diabetes Care. 2006 Jul;29(7):1613-8. doi: 10.2337/dc05-1711.
We sought to assess the risk of progression to type 2 diabetes in normal glucose tolerance (NGT) subjects based on the relationship between the plasma glucose concentration during oral glucose tolerance tests (OGTTs) and the fasting plasma glucose (FPG) concentration.
Subjects with NGT (n = 1,282) from the San Antonio Heart Study received an OGTT with measurement of the plasma glucose concentration at 0, 30, 60, and 120 min at baseline and after 7-8 years of follow-up. Subjects were divided into four groups based on the relationship between the plasma glucose concentration during the OGTT and the FPG concentration on the same day as the OGTT. Insulin resistance was calculated by the homeostasis model assessment of insulin resistance (HOMA-IR) and Matsuda index. Early-phase insulin secretion was calculated as the ratio between the incremental plasma insulin and glucose concentrations during the first 30 min of the OGTT (DeltaI(0-30)/DeltaG(0-30)). Total insulin secretion was calculated as the ratio between the incremental areas under the insulin and glucose curves during the OGTT [DeltaG(AUC)/DeltaI(AUC)].
In 23 subjects (group I), the plasma glucose concentration during the OGTT returned to levels below the FPG concentration at 30 min; in 111 subjects (group II) and in 313 subjects (group III), the plasma glucose concentration during the OGTT returned to levels below the FPG concentration at 60 and 120 min, respectively. In the remaining 835 subjects (group IV), the plasma glucose concentration during the OGTT never fell below the FPG concentration. Insulin resistance, measured by HOMA-IR and the Matsuda index, increased progressively from group I through group IV, while insulin secretion measured by DeltaI(0-30)/DeltaG(0-30) and DeltaG(AUC)/DeltaI(AUC) decreased progressively from group I through group IV. The incidence of type 2 diabetes was 0% in group I and progressively increased to 0.9% in group II, 3.2% in group III, and 6.4% in group IV.
Subjects whose postload plasma glucose concentration returned to baseline (i.e., FPG level) more quickly had greater insulin sensitivity, a higher insulinogenic index, and a lower risk of developing type 2 diabetes after 8 years of follow-up compared with subjects whose postload glucose concentration returned to baseline more slowly.
我们试图基于口服葡萄糖耐量试验（OGTT）期间的血浆葡萄糖浓度与空腹血糖（FPG）浓度之间的关系，评估正常糖耐量（NGT）受试者进展为2型糖尿病的风险。
来自圣安东尼奥心脏研究的NGT受试者（n = 1282）在基线时以及随访7 - 8年后接受了OGTT，并测量了0、30、60和120分钟时的血浆葡萄糖浓度。根据OGTT期间的血浆葡萄糖浓度与OGTT当天FPG浓度之间的关系，将受试者分为四组。通过胰岛素抵抗稳态模型评估（HOMA - IR）和松田指数计算胰岛素抵抗。将OGTT最初30分钟内血浆胰岛素和葡萄糖浓度的增量之比（DeltaI(0 - 30)/DeltaG(0 - 30)）计算为早期胰岛素分泌。将OGTT期间胰岛素和葡萄糖曲线下增量面积之比[DeltaG(AUC)/DeltaI(AUC)]计算为总胰岛素分泌。
在23名受试者（I组）中，OGTT期间的血浆葡萄糖浓度在30分钟时恢复到低于FPG浓度的水平；在111名受试者（II组）和313名受试者（III组）中，OGTT期间的血浆葡萄糖浓度分别在60分钟和120分钟时恢复到低于FPG浓度的水平。在其余835名受试者（IV组）中，OGTT期间的血浆葡萄糖浓度从未降至FPG浓度以下。通过HOMA - IR和松田指数测量的胰岛素抵抗从I组到IV组逐渐增加，而通过DeltaI(0 - 30)/DeltaG(0 - 30)和DeltaG(AUC)/DeltaI(AUC)测量的胰岛素分泌从I组到IV组逐渐减少。2型糖尿病的发病率在I组为0%，在II组逐渐增加到0.9%，在III组为3.2%，在IV组为6.4%。
与负荷后血糖浓度恢复到基线较慢的受试者相比，负荷后血浆葡萄糖浓度恢复到基线（即FPG水平）更快的受试者在随访8年后具有更高的胰岛素敏感性、更高的胰岛素生成指数和更低的发生2型糖尿病的风险。
