Lautamäki Riikka, Airaksinen K E Juhani, Seppänen Marko, Toikka Jyri, Luotolahti Matti, Ball Elizabeth, Borra Ronald, Härkönen Risto, Iozzo Patricia, Stewart Murray, Knuuti Juhani, Nuutila Pirjo
Turku PET Centre, Turku University Central Hospital, Kiinamyllynkatu 4-8, P.O. Box 52, FIN-20521 Turku, Finland.
Diabetes. 2005 Sep;54(9):2787-94. doi: 10.2337/diabetes.54.9.2787.
Rosiglitazone therapy improves insulin sensitivity and glucose uptake in patients with uncomplicated type 2 diabetes. In coronary artery disease (CAD), glucose is an important source of energy and preserved myocardial glucose uptake is essential for the viability of jeopardized myocardium. The aim was to test whether rosiglitazone changes myocardial metabolism in type 2 diabetic patients with CAD. We studied 54 patients (38 men and 16 women) with type 2 diabetes (HbA(1c) 7.2 + 0.9%) and CAD. Myocardial glucose uptake was measured with [(18)F]fluoro-2-deoxy-d-glucose positron emission tomography in ischemic (evaluated by single-photon emission tomography and coronary angiography) and nonischemic regions during euglycemic-hyperinsulinemic clamp before and after a 16-week intervention period with rosiglitazone (n = 27) or placebo (n = 27). Rosiglitazone significantly improved glycemic control (P < 0.0001) and whole-body insulin sensitivity (P < 0.0001). Rosiglitazone increased myocardial glucose uptake from 20.6 +/- 11.8 to 25.5 +/- 12.4 micromol . 100 g(-1) . min(-1) (P = 0.038 vs. baseline, P = 0.023 vs. placebo) in ischemic regions and from 21.7 +/- 12.1 to 28.0 +/- 12.7 micromol . 100 g(-1) . min(-1) (P = 0.014 vs. baseline, P = 0.003 vs. placebo) in nonischemic regions. The increase in myocardial glucose uptake was partly explained by the suppression of free fatty acid levels during clamp. Rosiglitazone therapy significantly increased insulin sensitivity and improved myocardial glucose uptake in type 2 diabetic patients with CAD. These results suggest that rosiglitazone therapy may facilitate myocardial glucose storage and utilization in these patients.
罗格列酮治疗可改善无并发症的2型糖尿病患者的胰岛素敏感性和葡萄糖摄取。在冠状动脉疾病（CAD）中，葡萄糖是重要的能量来源，维持心肌葡萄糖摄取对于濒危心肌的存活至关重要。目的是测试罗格列酮是否会改变2型糖尿病合并CAD患者的心肌代谢。我们研究了54例2型糖尿病（糖化血红蛋白[HbA(1c)] 7.2 + 0.9%）合并CAD的患者（38例男性和16例女性）。在使用罗格列酮（n = 27）或安慰剂（n = 27）进行16周干预期前后，通过正电子发射断层扫描用[18F]氟-2-脱氧-d-葡萄糖在正常血糖-高胰岛素钳夹期间测量缺血（通过单光子发射断层扫描和冠状动脉造影评估）和非缺血区域的心肌葡萄糖摄取。罗格列酮显著改善了血糖控制（P < 0.0001）和全身胰岛素敏感性（P < 0.0001）。罗格列酮使缺血区域的心肌葡萄糖摄取从20.6±11.8增加至25.5±12.4 μmol·100 g-1·min-1（与基线相比P = 0.038，与安慰剂相比P = 0.023），使非缺血区域的心肌葡萄糖摄取从21.7±12.1增加至28.0±12.7 μmol·100 g-1·min-1（与基线相比P = 0.014，与安慰剂相比P = 0.003）。心肌葡萄糖摄取的增加部分归因于钳夹期间游离脂肪酸水平的抑制。罗格列酮治疗显著提高了2型糖尿病合并CAD患者的胰岛素敏感性并改善了心肌葡萄糖摄取。这些结果表明，罗格列酮治疗可能有助于这些患者的心肌葡萄糖储存和利用。
