Nian Xiaoping, Sun Gaisheng, Dou Chunmei, Hou Hongbo, Fan Xiuping, Yu Hongmei, Ma Ling, He Bingxian
Department of Medicine, Baijiantan Hospital, Klamayi, Xinjiang Uigur Autonomous Region, China.
Zhonghua Yi Xue Za Zhi. 2002 Jun 10;82(11):732-5.
To investigate the influence of insulin resistance and pancreatic beta-cell function on plasma glucose level in type 2 diabetes so as to provide theoretical basis for reasonable selection of hypoglycemic agents.
The plasma non-specific insulin (NSINS), true insulin (TI) and glucose in eight-one type 2 diabetics, 38 males and 43 females, with a mean age of 53 years, were examined 0, 30, 60 and 120 minutes after they had 75 grams of instant noodles. The patients were divided into two groups according to their fasting plasma glucose (FPG): group A (FPG < 8.89 mmol/L) and group B (FPG> = 8.89 mmol/L). The insulin resistance was evaluated by HOMA-IR, the beta-cell function was evaluated by HOMA-beta formula and the formula deltaI(30)/deltaG(30) = (deltaI(30)-deltaI(0))/(deltaG(30)-deltaG(0)). The insulin area under curve (INSAUC) was evaluated by the formula INSAUC=FINS/2+INS(30)+INS(60)+INS(120)/2.
The mean FPG was 6.23 mmol/L in group A and 12.6 mmol/L in group B. PG2H was 11.7 mmol/L in group A and 19.2 mmol/L in group B. The TI levels in group B at 0, 30, 60, 120 min during standard meal test were significantly higher than those in group A: 6.15 +/- 1.06 vs 4.77 +/- 1.06, 9.76 +/- 1.1 vs 5.88 +/- 1.1,14.68 +/- 1.11 vs 6.87 +/- 1.1 and 17.13 +/- 1.12 vs 8.0 +/- 1.1 microU/dl (all P< 0.01). The NSINS showed the same trend. The insulin resistance in group B was 1.5 times that in group A. With the insulin resistance adjusted, the beta cell function in group A was 5 to 6 times that in group B. The INSAUC in group A was 1.66 times larger than that in group B, especially the INSAUC for true insulin (2 times larger). The contribution of insulin resistance and beta cell function to PG2H was half by half in group A and 1:8 in group B. beta cell function calculated by insulin (Homa-beta) explained 41% of the plasma glucose changes in group A and 54% of the plasma glucose changes in group B. The contribution of insulin deficiency to plasma glocose was 3.3.times that of insulin resistance in group A and was 9.5 times that of insulin resistance in group B. Insulin sensitivity explained 12% of the plasma glucose changes in group A, and only 5.7% of the plasma glucose changes in group B.
Diabetics with FPG greater than 8.89 mmol/L have both higher insulin resistance and poorer beta-cell function, their hyperglycemia being caused mainly by beta-cell failure, The combined use of insulin sensitizer and insulin or insulintropic agents during the initial stage of treatment is effective.
探讨胰岛素抵抗和胰岛β细胞功能对2型糖尿病患者血糖水平的影响，为合理选用降糖药物提供理论依据。
对81例2型糖尿病患者（男38例，女43例，平均年龄53岁）口服75克方便面后0、30、60及120分钟检测血浆非特异性胰岛素（NSINS）、真胰岛素（TI）及血糖。根据空腹血糖（FPG）将患者分为两组：A组（FPG＜8.89 mmol/L）和B组（FPG≥8.89 mmol/L）。采用HOMA-IR评估胰岛素抵抗，用HOMA-β公式及公式deltaI(30)/deltaG(30) = (deltaI(30)-deltaI(0))/(deltaG(30)-deltaG(0))评估β细胞功能。用公式INSAUC=FINS/2+INS(30)+INS(6)+INS(120)/2评估胰岛素曲线下面积（INSAUC）。
A组平均FPG为6.23 mmol/L，B组为12.6 mmol/L。A组服糖后2小时血糖（PG2H）为11.7 mmol/L，B组为19.2 mmol/L。标准餐试验中，B组0、30、60、120分钟时TI水平显著高于A组：6.15±1.06对4.77±1.06、9.76±1.1对5.88±1.1、14.68±,1对6.87±1.1及17.13±1.12对8.0±1.1 μU/dl（均P＜0.01）。NSINS呈现相同趋势。B组胰岛素抵抗是A组的1.5倍。校正胰岛素抵抗后，A组β细胞功能是B组的5至6倍。A组INSAUC比B组大1.66倍，尤其是真胰岛素的INSAUC（大2倍）。A组胰岛素抵抗和β细胞功能对PG2H的贡献各占一半，B组为1:8。胰岛素（Homa-β）计算的β细胞功能在A组解释了41%的血糖变化，在B组解释了54%的血糖变化。A组胰岛素缺乏对血糖的贡献是胰岛素抵抗的3.3倍，B组是胰岛素抵抗的9.5倍。胰岛素敏感性在A组解释了12%的血糖变化，在B组仅解释了5.7%的血糖变化。
FPG大于8.89 mmol/L的糖尿病患者胰岛素抵抗较高且β细胞功能较差，其高血糖主要由β细胞功能衰竭所致，治疗初期联合使用胰岛素增敏剂和胰岛素或促胰岛素分泌剂有效。
