Trials for the evaluation of hepatic insulin resistance with novel simplified method using platelet

我们使用高胰岛素正糖钳法和我们的血小板聚集简化法检查60例慢性肝病患者的胰岛素敏感性，因为我们注意到在另一项研究中，使用血小板简化法评估的肝硬化患者的胰岛素敏感性往往是正常的。因此，血小板简化法只能反映外周组织的胰岛素抵抗，而不能反映肝组织的胰岛素抵抗。我们发现，在高胰岛素正糖钳夹（夹子- ogl -CPR法）中，c肽（CPR）对口服葡萄糖负荷的反应可以评价门脉糖传感器（PGS）的功能。我们测量了30名糖尿病患者、10名患有IGT的肥胖受试者、10名糖耐量正常的肥胖受试者和10名作为对照的正常受试者的CPR反应。伴有或不伴有肥胖的糖尿病患者和伴有IGT的肥胖患者的心肺复苏术反应显著降低或完全不存在，而伴有葡萄糖耐受不良（单纯性肥胖）的肥胖患者的心肺复苏术反应良好。肝硬化患者钳型- ogl -CPR与糖尿病患者相似，其心肺复苏术反应明显降低。我们认为PGS紊乱可能不仅与糖尿病患者餐后高血糖有关，也与肝硬化患者餐后高血糖有关，而与胰岛素抵抗无关。目前，我们在2型糖尿病动物模型中研究了PGS功能与葡萄糖耐受不良的关系。在另一项研究中，我们明确瘦素可以增加胰岛素刺激的外周组织的葡萄糖摄取，而不是肝组织。

We examined insulin sensitivity in 60 patients with chronic liver disease using hyperinsulinemic euglycemic clamp method and our simplified method by platelet aggregation, because we noticed that insulin sensitivity in cirrhotic patients evaluated by simplified method using platelet was tend to be in normal in the other study. So we concluded that simplified method using platelet could reflect insulin resistance only in the peripheral tissues but not in the liver tissue. We found that the C-peptide (CPR) response to oral glucose load during hyperinsulinemic euglycemic clamp (clamp-OGL-CPR method) could evaluate the function of portal glucosensor (PGS). We measured CPR response in 30 diabetics, 10 obese subjects with IGT and 10 obese subjects with normal glucose tolerance and 10 normal subjects as control. The CPR response in the diabetics with or without obesity and obese subjects with IGT was remarkably reduced or completely absent nevertheless that in obese subjects without glucose intolerance (simple obesity) was good. CPR response in the patients with liver cirrhosis during clamp-OGL-CPR method was remarkably reduced like diabetic patient. We supposed that the disorders in PGS might be related to postprandial hyperglycemia not only in diabetics but also in the patients with liver cirrhosis, and could not relate to insulin resistance. Now we have been examining the relation between the function of PGS and the glucose intolerance in the animal model of type 2 diabetes. In other study, we made clear that leptin could increase insulin-stimulated glucose uptake in the peripheral tissues but not in liver tissue.