Division of Endocrinology & Metabolism, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Diabetes Metab Res Rev. 2011 May;27(4):354-61. doi: 10.1002/dmrr.1183.
Individual effects of hyperglycaemia and obesity to impair vascular health are recognized. However, the relative contributions of dysglycaemia versus other obesity-related traits to vascular dysfunction have not been systematically evaluated.
We undertook a cross-sectional evaluation of factors contributing to vascular function in 271 consecutive subjects, categorized as non-obese normal glucose tolerant (n = 115), non-obese dysglycaemic (n = 32), obese normal glucose tolerant (n = 57), obese dysglycaemic (n = 38), or type 2 diabetic (n = 29). Vascular function was measured invasively as leg blood flow responses to methacholine chloride, an endothelium-dependent vasodilator. Categorical and continuous analyses were carried out to assess the contributions of hyperglycaemia to vascular dysfunction.
Even among normoglycaemic subjects, obese subjects had impaired vascular function compared to non-obese subjects (p = 0.004). Vascular function was also impaired in non-obese dysglycaemic subjects (p = 0.04 versus non-obese normoglycaemic subjects), to a level comparable to normoglycaemic obese subjects. Within obese subject groups, gradations of dysglycaemia including the presence of diabetes were not associated with further worsening of these vascular responses beyond the effect of obesity alone (p = not significant comparing all obese groups, p < 0.001 versus lean normoglycaemic subjects). After univariate and multivariable modelling analyses we found that effects of glycaemia were less powerful than effects of insulin resistance and obesity on vascular dysfunction.
Dysglycaemia contributes to impaired vascular function in non-obese subjects, but obesity and insulin resistance are more important determinants of vascular function in obese and diabetic subjects.
高血糖和肥胖对血管健康的个体影响已得到认可。然而,血糖异常与其他肥胖相关特征对血管功能障碍的相对贡献尚未得到系统评估。
我们对 271 例连续患者的血管功能相关因素进行了横断面评估,这些患者被分为非肥胖糖耐量正常(n=115)、非肥胖糖代谢异常(n=32)、肥胖糖耐量正常(n=57)、肥胖糖代谢异常(n=38)或 2 型糖尿病(n=29)。血管功能通过氯甲酰甲胆碱(一种内皮依赖性血管扩张剂)引起的腿部血流反应进行侵入性测量。进行了分类和连续分析,以评估高血糖对血管功能障碍的贡献。
即使在血糖正常的患者中,肥胖患者的血管功能也比非肥胖患者受损(p=0.004)。非肥胖糖代谢异常患者的血管功能也受损(p=0.04 与非肥胖糖耐量正常患者相比),与糖耐量正常的肥胖患者相当。在肥胖患者组内,包括糖尿病在内的不同程度的糖代谢异常与肥胖单独作用以外的血管反应进一步恶化无关(p=各组间无显著差异,p<0.001 与瘦糖耐量正常患者相比)。在单变量和多变量模型分析后,我们发现血糖的影响不如胰岛素抵抗和肥胖对血管功能障碍的影响强大。
糖代谢异常导致非肥胖患者血管功能受损,但肥胖和胰岛素抵抗是肥胖和糖尿病患者血管功能的更重要决定因素。