Shinozaki K, Suzuki M, Ikebuchi M, Hara Y, Harano Y
Department of Medicine, National Cardiovascular Center, Osaka, Japan.
Diabetes Care. 1996 Jan;19(1):1-7. doi: 10.2337/diacare.19.1.1.
To evaluate the relation between insulin resistance and coronary atherosclerosis, insulin sensitivity in lean nondiabetic, normotensive subjects with and without obstructive coronary artery disease (CAD). The correlation between insulin resistance and degree of coronary stenosis was also investigated.
Four groups were studied: 1) nine subjects with normal glucose tolerance (NGT) without CAD, 2) 10 subjects with NGT with CAD, 3) nine subjects with impaired glucose tolerance (IGT) without CAD, and 4) 10 subjects with IGT with CAD. Insulin sensitivity was determined by the steady-state plasma glucose (SSPG) method using Sandostatin. Coronary angiography was performed in all study subjects, and the severity of coronary artery atherosclerosis was quantified in a modified Gensini score.
The SSPG (millimoles per liter) levels were significantly higher in the patients with CAD compared with control subjects (control vs. patient group: 4.8 +/- 0.5 vs. 7.9 +/- 0.9 with NGT, P < 0.05; 5.6 +/- 0.5 vs. 11.1 +/- 0.8 with IGT, P < 0.001), indicating the presence of insulin resistance in patients with CAD. The coronary atherosclerosis score (CAS) was significantly and positively correlated with SSPG (r = 0.74, P < 0.05) and 2-h insulin area (r = 0.78, P < 0.01) in NGT subjects with CAD. On the other hand, the percentage fall of plasma free fatty acid (0-30 min) during an insulin sensitivity test was significantly decreased in the subjects with CAD and was inversely correlated with the CAS (r = -0.43, P < 0.05), especially in NGT subjects with CAD.
These data suggest that in patients with CAD, insulin-mediated glucose metabolism is significantly impaired, and a significant correlation was noted between insulin resistance and severity of CAD. Therefore, the hyperinsulinemia often observed in patients with CAD is attributable to the compensatory mechanism of the beta-cell to the inadequate action of insulin for glucose metabolism. Hyperinsulinemia in the presence of insulin resistance aggravates dyslipidemia and may stimulate the atheromatous process by an as-yet-unknown mechanism.
评估胰岛素抵抗与冠状动脉粥样硬化之间的关系，以及在无阻塞性冠状动脉疾病（CAD）和有CAD的非糖尿病、血压正常的瘦人受试者中的胰岛素敏感性。同时研究胰岛素抵抗与冠状动脉狭窄程度之间的相关性。
共研究四组：1）9名糖耐量正常（NGT）且无CAD的受试者；2）10名NGT且有CAD的受试者；3）9名糖耐量受损（IGT）且无CAD的受试者；4）10名IGT且有CAD的受试者。使用善宁通过稳态血浆葡萄糖（SSPG）法测定胰岛素敏感性。对所有研究对象进行冠状动脉造影，并采用改良的Gensini评分对冠状动脉粥样硬化的严重程度进行量化。
与对照组相比，CAD患者的SSPG（毫摩尔/升）水平显著更高（对照组与患者组：NGT时为4.8±0.5对7.9±0.9，P<0.05；IGT时为5.6±0.5对11.1±0.8，P<0.001），表明CAD患者存在胰岛素抵抗。在有CAD的NGT受试者中，冠状动脉粥样硬化评分（CAS）与SSPG（r = 0.74，P<0.05）和2小时胰岛素面积（r = 0.78，P<0.01）显著正相关。另一方面，在胰岛素敏感性试验期间，CAD受试者血浆游离脂肪酸（0 - 30分钟）的下降百分比显著降低，且与CAS呈负相关（r = -0.43，P<0.05），尤其是在有CAD的NGT受试者中。
这些数据表明在CAD患者中，胰岛素介导的葡萄糖代谢显著受损，且胰岛素抵抗与CAD严重程度之间存在显著相关性。因此，CAD患者中经常观察到的高胰岛素血症归因于β细胞对胰岛素葡萄糖代谢作用不足的代偿机制。存在胰岛素抵抗时的高胰岛素血症会加重血脂异常，并可能通过一种尚不清楚的机制刺激动脉粥样硬化进程。
