Wang P W, Abbasi F, Carantoni M, Chen Y D, Azhar S, Reaven G M
Stanford University School of Medicine, California 94305, USA.
J Clin Endocrinol Metab. 1997 Oct;82(10):3221-4. doi: 10.1210/jcem.82.10.4053.
Plasma glucose, insulin, and proinsulin concentrations were measured before and after an oral glucose challenge in 57 nondiabetic individuals. In addition, insulin-mediated glucose disposal was estimated by determining the steady state plasma glucose (SSPG) concentration after a 180-min iv infusion of somatostatin, insulin, and glucose. The plasma glucose concentration after oral glucose administration was used to divide the population into those with normal (n = 36) or impaired glucose tolerance (IGT; n = 21), and the 36 normal glucose-tolerant individuals were further subdivided into an insulin-sensitive (SSPG, < 9.0 mmol/L; n = 15) and an insulin-resistant (SSPG, > 10 mmol/L; n = 21) group. Fasting and postglucose load insulin concentrations were similar in the normal glucose-tolerant insulin-resistant and IGT groups, but were significantly higher (P < 0.02- < 0.001) than those in normal glucose-tolerant insulin-sensitive individuals. Fasting proinsulin concentrations were also higher (P < 0.002) in the normal glucose-tolerant insulin-resistant (15.1 +/- 1.5 pmol/L) and IGT (15.8 +/- 1.8 pmol/L) groups compared to those in normal glucose-tolerant insulin-sensitive volunteers (9.3 +/- 1.2 pmol/ L). However, the ratio of fasting proinsulin to insulin was identical in all three groups (0.12). When the three groups were combined, significant relationships (P < 0.001) existed between SSPG (degree of insulin resistance) and both fasting proinsulin (r = 0.59) and insulin (r = 0.66) concentrations, but not with the ratio of proinsulin to insulin (r = 0.03). These results demonstrate that fasting proinsulin and insulin concentrations are increased in insulin-resistant, nondiabetic subjects, and the more insulin resistant, the greater the increase. In contrast, the ratio of proinsulin to insulin did not vary as a function of insulin resistance. Thus, neither insulin resistance nor the need to secrete more insulin to maintain glucose tolerance necessarily leads to abnormal insulin processing by the beta-cell.
对57名非糖尿病个体在口服葡萄糖激发试验前后测量了血浆葡萄糖、胰岛素和胰岛素原浓度。此外，通过在静脉输注生长抑素、胰岛素和葡萄糖180分钟后测定稳态血浆葡萄糖（SSPG）浓度来估计胰岛素介导的葡萄糖处置情况。根据口服葡萄糖后血浆葡萄糖浓度将人群分为葡萄糖耐量正常者（n = 36）和葡萄糖耐量受损者（IGT；n = 21），36名葡萄糖耐量正常个体进一步细分为胰岛素敏感组（SSPG，< 9.0 mmol/L；n = 15）和胰岛素抵抗组（SSPG，> 10 mmol/L；n = 21）。葡萄糖耐量正常的胰岛素抵抗组和IGT组的空腹及葡萄糖负荷后胰岛素浓度相似，但显著高于（P < 0.02 - < 0.001）葡萄糖耐量正常的胰岛素敏感个体。与葡萄糖耐量正常的胰岛素敏感志愿者（9.3 ± 1.2 pmol/L）相比，葡萄糖耐量正常的胰岛素抵抗组（15.1 ± 1.5 pmol/L）和IGT组（15.8 ± 1.8 pmol/L）的空腹胰岛素原浓度也更高（P < 0.002）。然而，三组的空腹胰岛素原与胰岛素比值相同（0.12）。当三组合并时，SSPG（胰岛素抵抗程度）与空腹胰岛素原（r = 0.59）和胰岛素（r = 0.66）浓度之间存在显著相关性（P < 0.001），但与胰岛素原与胰岛素的比值无关（r = 0.03）。这些结果表明，在胰岛素抵抗的非糖尿病受试者中，空腹胰岛素原和胰岛素浓度升高，胰岛素抵抗越严重，升高幅度越大。相反，胰岛素原与胰岛素的比值并不随胰岛素抵抗而变化。因此，无论是胰岛素抵抗还是为维持葡萄糖耐量而分泌更多胰岛素的需求，都不一定导致β细胞胰岛素加工异常。
