Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Wien, Austria.
Diabetologia. 2011 Jul;54(7):1871-8. doi: 10.1007/s00125-011-2146-0. Epub 2011 Apr 15.
AIMS/HYPOTHESIS: Insulin resistance, an independent risk-factor for cardiovascular disease, precedes type 2 diabetes and is associated with ectopic lipid accumulation in skeletal muscle and liver. Recent evidence indicates that cardiac steatosis plays a central role in the development of diabetic cardiomyopathy. However, it is not known whether insulin resistance as such in the absence of type 2 diabetes is associated with heart steatosis and/or impaired function. We therefore assessed myocardial steatosis and myocardial function in a sample of women with normal insulin sensitivity, insulin resistance, impaired glucose tolerance (IGT) and type 2 diabetes.
Magnetic resonance imaging and localised spectroscopy were used to measure left ventricular dynamic variables and myocardial lipid accumulation in interventricular septum of non-diabetic, age- and BMI-matched insulin-sensitive (n = 11, 47 ± 6 years, BMI 25 ± 2 kg/m(2); clamp-like index [CLIX] = 9.7 ± 0.7) and insulin-resistant (n = 10, 48 ± 5 years, 27 ± 4 kg/m(2); CLIX = 4.5 ± 0.4) women with normal glucose tolerance as well as of women with IGT (n = 6, 45 ± 5 years, 28 ± 6 kg/m(2); CLIX = 3.6 ± 1.1) and type 2 diabetes (n = 7, 52 ± 10 years, 27 ± 3 kg/m(2)).
Myocardial lipid content was increased in type 2 diabetic women only (insulin-sensitive 0.4 ± 0.2% [means ± SD]; insulin-resistant 0.4 ± 0.1%; IGT 0.5 ± 0.2%; type 2 diabetes 0.7 ± 0.3%; p < 0.05). In insulin-resistant and type 2 diabetic women, stroke volume was lower (-15% and -27%, respectively, vs insulin-sensitive) and heart rate was higher (11% and 14%, respectively, vs insulin-sensitive, p < 0.05). No other differences in systolic and diastolic function were observed between study groups.
CONCLUSIONS/INTERPRETATION: In contrast to liver and skeletal muscle, insulin resistance as such is not associated with increased myocardial lipid accumulation.
目的/假设：胰岛素抵抗是心血管疾病的独立危险因素，先于 2 型糖尿病发生，并与骨骼肌和肝脏的异位脂质积累有关。最近的证据表明，心脏脂肪变性在糖尿病心肌病的发展中起核心作用。然而，目前尚不清楚 2 型糖尿病以外的胰岛素抵抗本身是否与心脏脂肪变性和/或功能障碍有关。因此，我们评估了胰岛素敏感性正常、胰岛素抵抗、糖耐量受损（IGT）和 2 型糖尿病的女性样本中的心肌脂肪变性和心肌功能。
磁共振成像和局部光谱学用于测量非糖尿病、年龄和 BMI 匹配的胰岛素敏感（n=11，47±6 岁，BMI 25±2kg/m²；钳夹指数 [CLIX]=9.7±0.7）和胰岛素抵抗（n=10，48±5 岁，27±4kg/m²；CLIX=4.5±0.4）女性以及 IGT（n=6，45±5 岁，28±6kg/m²；CLIX=3.6±1.1）和 2 型糖尿病（n=7，52±10 岁，27±3kg/m²）患者的左心室动态变量和室间隔心肌脂质积累。
仅在 2 型糖尿病女性中观察到心肌脂质含量增加（胰岛素敏感组 0.4±0.2%[平均值±标准差]；胰岛素抵抗组 0.4±0.1%；IGT 组 0.5±0.2%；2 型糖尿病组 0.7±0.3%；p<0.05）。在胰岛素抵抗和 2 型糖尿病女性中，心排量降低（分别为-15%和-27%，与胰岛素敏感组相比），心率升高（分别为 11%和 14%，与胰岛素敏感组相比，p<0.05）。在各组之间未观察到收缩和舒张功能的其他差异。
结论/解释：与肝脏和骨骼肌不同，胰岛素抵抗本身与心肌脂质积累增加无关。
