Division of Metabolic and Cardiovascular Research, Health Professions Division, Nova Southeastern University, Fort Lauderdale, Florida 33328, USA.
Metab Syndr Relat Disord. 2012 Oct;10(5):344-50. doi: 10.1089/met.2012.0040. Epub 2012 Jul 17.
Metabolic syndrome, impaired fasting glucose (IFG), and impaired glucose tolerance (IGT) predict risk for type 2 diabetes mellitus (T2DM). To determine if increased risk preceded development of these abnormalities, β-cell function and insulin resistance were assessed in euglycemic subjects with and without traits of metabolic syndrome.
A total of 562 apparently healthy Latin-American subjects were screened for metabolic syndrome [National Education Cholesterol Program Adult Treatment Panel III (NECP ATP III)]. Early pancreatic insulin response ΔInsulin(0-30)/ΔGlucose(0-30), Matsuda index, disposition index (DI), and homeostasis model assessment of insulin resistance (HOMA-IR) ratio were obtained from oral glucose tolerance testing (0-180 min).
ΔI(0-30)/ΔG(0-30), Matsuda index, DI, and HOMA-IR deteriorated in direct proportion with number of traits of metabolic syndrome, and with increases in glucose levels within the euglycemic range. DI was the most sensitive index. In subjects with 1, 2, 3, and 4-5 traits, DI was 21.4%, 40%, 57%, and 76% lower, respectively, than in subjects with no traits. As a single trait, abdominal obesity was associated with insulin resistance, whereas, low high-density lipoprotein cholesterol (HDL-C), alone or combined with high triglycerides, was not associated with insulin resistance or β-cell dysfunction. Combined impairments in β-cell function and insulin sensitivity were responsible for the increases in fasting and 2-h plasma glucose concentrations within the euglycemic range.
Impaired β-cell function and increased insulin resistance are present much before development of metabolic syndrome, IFG, or IGT. β-Cell function and insulin sensitivity worsen in direct proportion with number of traits of metabolic syndrome and increases in glucose levels. Compared to abdominal obesity, low HDL-C±high triglycerides may bear a lesser weight in predicting risk of T2DM.
代谢综合征、空腹血糖受损（IFG）和葡萄糖耐量受损（IGT）可预测 2 型糖尿病（T2DM）的发病风险。为了确定这些异常发生前是否存在风险增加，我们评估了代谢综合征伴或不伴相关特征的血糖正常受试者的胰岛β细胞功能和胰岛素抵抗。
总共对 562 名拉丁美洲的貌似健康的个体进行了代谢综合征筛查[国家胆固醇教育计划成人治疗小组第三次报告（NECP ATP III）]。通过口服葡萄糖耐量试验（0-180 分钟）获得了胰岛早期胰岛素反应（0-30 分钟时的胰岛素变化量与 0-30 分钟时的血糖变化量之比，ΔInsulin(0-30)/ΔGlucose(0-30)）、Matsuda 指数、胰岛β细胞功能指数（DI）和稳态模型评估的胰岛素抵抗指数（HOMA-IR）比值。
随着代谢综合征特征数量的增加，以及血糖在正常范围内升高，ΔI(0-30)/ΔG(0-30)、Matsuda 指数、DI 和 HOMA-IR 呈比例恶化。DI 是最敏感的指标。在具有 1、2、3 和 4-5 种特征的个体中，与不具有特征的个体相比，DI 分别低 21.4%、40%、57%和 76%。作为单一特征，腹部肥胖与胰岛素抵抗相关，而单独或联合存在高甘油三酯的低高密度脂蛋白胆固醇（HDL-C）与胰岛素抵抗或胰岛β细胞功能障碍无关。在正常血糖范围内，胰岛β细胞功能和胰岛素敏感性的联合损害导致空腹和 2 小时血糖浓度的升高。
在代谢综合征、IFG 或 IGT 发生之前，就已经存在胰岛β细胞功能受损和胰岛素抵抗增加。随着代谢综合征特征数量的增加和血糖水平的升高，胰岛β细胞功能和胰岛素敏感性呈比例恶化。与腹部肥胖相比，低 HDL-C±高甘油三酯可能在预测 T2DM 风险方面的作用较小。
