Section of Endocrinology, Department of Clinical Pathophysiology, University of Florence, Italy.
Diabet Med. 2011 Oct;28(10):1229-33. doi: 10.1111/j.1464-5491.2011.03332.x.
To determine the association between the hypertriglyceridaemic waist phenotype, a combination of enlarged waist circumference and increased triglyceride levels, and β-cell function in subjects with normal glucose tolerance and those with impaired glucose tolerance.
We studied 1344 outpatients clinic without diabetes. Overnight fasting blood samples were obtained to measure plasma glucose, insulin and lipids. An oral glucose tolerance test was performed in all subjects. All patients were divided in four groups, two groups with normal glucose tolerance and two with impaired glucose tolerance, with or without the hypertriglyceridaemic waist phenotype. Insulin resistance and β-cell function were calculated by homeostatsis model assessment 2 indices.
Twenty per cent of subjects showed the hypertriglyceridaemic waist phenotype and 23.8% had impaired glucose tolerance. We found a progressive significant increase (P < 0.001) of insulin resistance from subjects with normal glucose tolerance without the hypertriglyceridaemic waist phenotype with respect to patients with impaired glucose tolerance with the hypertriglyceridaemic waist phenotype. In subjects with normal glucose tolerance, the hypertriglyceridaemic waist phenotype was associated with a mild, but not significant, increase of homeostatsis model assessment 2-β levels; but, in patients with impaired glucose tolerance, the hypertriglyceridaemic waist phenotype was associated with significantly lower homeostatsis model assessment 2-β levels [127.0 (103.0-162.7) vs. 123.0 (96.0-147.0); P < 0.05]. The hypertriglyceridaemic waist phenotype displayed a higher (odds ratio 95% CI) β-cell dysfunction of 1.8 (1.3-2.6) and insulin resistance of 5.0 (2.7-8.5) compared with 1.3 (0.9-1.9) and 2.4 (1.8-3.2), respectively, of waist circumference alone.
In this study, the hypertriglyceridaemic waist phenotype is associated with increased insulin resistance and an overstimulation of β-cell function in subjects with normal glucose tolerance, while patients with impaired glucose tolerance with the hypertriglyceridaemic waist phenotype showed a reduction in β-cell function. These data suggest the importance of the identification of patients with impaired glucose tolerance combined with the hypertriglyceridaemic waist phenotype for an early intervention in relation to the high risk of developing Type 2 diabetes.
确定高甘油三酯腰围表型（腰围增大和甘油三酯水平升高的组合）与糖耐量正常和糖耐量受损患者的β细胞功能之间的关联。
我们研究了 1344 名无糖尿病的门诊患者。采集 overnight fasting 血样以测量血浆葡萄糖、胰岛素和脂质。所有患者均进行口服葡萄糖耐量试验。所有患者均分为四组，两组糖耐量正常，两组糖耐量受损，有无高甘油三酯腰围表型。采用稳态模型评估 2 指数计算胰岛素抵抗和β细胞功能。
20%的患者存在高甘油三酯腰围表型，23.8%的患者糖耐量受损。我们发现，与无高甘油三酯腰围表型的糖耐量正常患者相比，糖耐量受损且存在高甘油三酯腰围表型的患者胰岛素抵抗呈进行性显著增加（P<0.001）。在糖耐量正常的患者中，高甘油三酯腰围表型与稳态模型评估 2-β水平的轻度但无显著性升高相关；但是，在糖耐量受损的患者中，高甘油三酯腰围表型与显著较低的稳态模型评估 2-β水平相关[127.0（103.0-162.7）vs. 123.0（96.0-147.0）；P<0.05]。与单独腰围相比，高甘油三酯腰围表型显示出更高的（比值比 95%置信区间）β细胞功能障碍 1.8（1.3-2.6）和胰岛素抵抗 5.0（2.7-8.5）。
在这项研究中，高甘油三酯腰围表型与糖耐量正常患者的胰岛素抵抗增加和β细胞功能过度刺激相关，而存在高甘油三酯腰围表型的糖耐量受损患者的β细胞功能降低。这些数据表明，识别糖耐量受损合并高甘油三酯腰围表型的患者对于早期干预与 2 型糖尿病发生风险较高有关。
