Duman B Susleyici, Turkoglu C, Gunay D, Cagatay P, Demiroglu C, Buyukdevrim A Sevim
Department of Medical Biology and Genetics, Kadir Has University, School of Medicine, Vefa Bey Sok. No. 5, 80810-Gayrettepe-Istanbul, Turkey.
Diabetes Nutr Metab. 2003 Aug;16(4):243-50.
This paper investigates the relative role of the impairment of insulin secretion and action in the pathogenesis of Type 2 diabetes mellitus (T2DM). The parameters indicating insulin secretion and action were calculated from the data obtained during oral glucose tolerance test (OGTT), in 156 age- and sex-matched T2DM patients divided in 4 groups according to their body mass index (BMI, I = 20.0-24.9, II = 25.0-29.9, III = 30.0-39.9 and IV > 40.0 kg/m2). After obtaining baseline biomedical parameters (plasma glucose, serum insulin, cholesterol, HDL-cholesterol, triglycerides, BMI, and amount of fat tissue), the rates of insulin secretory capacity and insulin action were obtained from OGTT and compared between the T2DM patients with normal body weight and different grades of obesity. Beta-cell secretory capacity of the participants was found to be proportionally and significantly higher in graded obese than that of the normal body weight patients. The rates of hepatic as well as peripheral insulin resistance in obese groups proportionally and significantly rise in comparison with that of non-obese diabetics. In addition, these parameters are shown to be related to the body fat, presumably visceral in origin. In conclusion, hyperglycemia-hyperinsulinemia observed in obese and T2DM patients might be due, in part, to increased capacity of insulin secretion, and to exaggerated hepatic glucose production because of hepatic insulin resistance, respectively.
本文研究胰岛素分泌和作用受损在2型糖尿病(T2DM)发病机制中的相对作用。根据口服葡萄糖耐量试验(OGTT)获得的数据,计算156例年龄和性别匹配的T2DM患者胰岛素分泌和作用的参数,这些患者根据体重指数(BMI,I = 20.0 - 24.9,II = 25.0 - 29.9,III = 30.0 - 39.9,IV > 40.0 kg/m²)分为4组。在获得基线生物医学参数(血糖、血清胰岛素、胆固醇、高密度脂蛋白胆固醇、甘油三酯、BMI和脂肪组织量)后,从OGTT中获得胰岛素分泌能力和胰岛素作用的速率,并在正常体重和不同肥胖程度的T2DM患者之间进行比较。发现分级肥胖参与者的β细胞分泌能力比正常体重患者成比例且显著更高。与非肥胖糖尿病患者相比,肥胖组的肝脏和外周胰岛素抵抗率成比例且显著升高。此外,这些参数显示与身体脂肪有关,推测起源于内脏。总之,肥胖和T2DM患者中观察到的高血糖 - 高胰岛素血症可能分别部分归因于胰岛素分泌能力增加以及由于肝脏胰岛素抵抗导致的肝脏葡萄糖生成增加。