Inoue S, Ota M, Iizuka T, Murao S
Jpn Heart J. 1975 Nov;16(6):670-82. doi: 10.1536/ihj.16.670.
Blood glucose, free fatty acid and insulin responses to oral glucose and the fasting serum lipids were measured in 3 groups: 32 non-obese (mean age: 47.5 years) and 9 obese (mean age: 84.5 years), male patients with coronary heart disease and 12 non-obese male controls (mean age: 46.5 years). The oral glucose tolerance tests were repeated after 3 years in 16 of the non-obese patients with coronary heart disease. The results were as follows: 1) Glucose tolerance was impaired in 19 of 32 non-obese patients (59.4%). There was a significant correlation between impaired glucose tolerance and hyperlipidemia (hypercholesterolemia and/or hypertriglyceridemia). 2) In obese patients FFA levels at 30, 60, and 120 min after oral glucose administration were significantly elevated and FFA decrease was delayed with a drop to minimum levels at 180 min. 3) The insulin response after oral glucose administration in the group of non-obese patients with normal glucose tolerance was similar to that of non-obese controls. In the group of non-obese patients with impaired glucose tolerance, serum insulin levels went up to normal levels, but the peak was delayed. The serum insulin levels in obese patients were significantly higher than those of controls of 0, 60, 120, and 180 min. After 3 years the change in insulin response to oral glucose was not related to anginal symptoms or ECG findings, but was related to body weight change in patients with minor changes in glucose tolerance. 4) The metabolic pattern in the non-obese group with impaired glucose tolerance resembled that of "mild diabetes" in delayed response of insulin and FFA, and mild hyperlipidemia. These findings suggest that obesity may contribute to hyperinsulinemia in patients with coronary heart disease and that impaired glucose tolerance observed in patients with coronary heart disease is in part due to "latent diabetes".
对3组人群进行了如下测量:口服葡萄糖后血糖、游离脂肪酸和胰岛素的反应以及空腹血脂,这3组人群分别为:32名非肥胖男性冠心病患者(平均年龄:47.5岁)、9名肥胖男性冠心病患者(平均年龄:84.5岁)和12名非肥胖男性对照者(平均年龄:46.5岁)。3年后,对16名非肥胖冠心病患者重复进行口服葡萄糖耐量试验。结果如下:1)32名非肥胖患者中有19名(59.4%)糖耐量受损。糖耐量受损与高脂血症(高胆固醇血症和/或高甘油三酯血症)之间存在显著相关性。2)肥胖患者口服葡萄糖后30、60和120分钟时的游离脂肪酸水平显著升高,游离脂肪酸下降延迟,在180分钟时降至最低水平。3)糖耐量正常的非肥胖患者组口服葡萄糖后的胰岛素反应与非肥胖对照组相似。糖耐量受损的非肥胖患者组中,血清胰岛素水平升至正常水平,但峰值延迟。肥胖患者在0、60、120和180分钟时的血清胰岛素水平显著高于对照组。3年后,口服葡萄糖的胰岛素反应变化与心绞痛症状或心电图结果无关,但与糖耐量有轻微变化的患者的体重变化有关。4)糖耐量受损的非肥胖组的代谢模式在胰岛素和游离脂肪酸反应延迟以及轻度高脂血症方面类似于“轻度糖尿病”。这些发现表明,肥胖可能导致冠心病患者出现高胰岛素血症,冠心病患者中观察到的糖耐量受损部分归因于“潜在糖尿病”。