老年肥胖者高三酰甘油血症与胰岛素抵抗

Hypertriglyceridemia and insulin resistance in the obese elderly

目的测定老年单纯肥胖者、肥胖和糖耐量受损（IGT）患者、肥胖和2型糖尿病（T2DM）患者及健康人外周血三酰甘油（TG）水平变化，探讨高TG血症在胰岛素抵抗中的作用。方法将82名受试对象分为单纯肥胖组、IGT肥胖组、T2DM肥胖组与健康对照组。测身高、体质量、血压、空腹血糖（FPG）、血TG、血胆固醇（TC）；采用放射免疫法（RIA）测定空腹胰岛素水平（FPI），并计算稳态模型评价胰岛素抵抗指数（HOMA-IR）。结果单纯肥胖组、IGT肥胖组、T2DM肥胖组血TG明显高于健康对照组[分别为（1．3±0．6）、（1．9±0．9）、（2．1±0．7）mmol／L与（1．0±0．2）mmol／L，均P〈0．05]，且肥胖程度相同的IGT肥胖组、T2DM肥胖组比单纯肥胖组TG水平明显升高[分别为（1．9±0．9）、（2．1±0．7）mmol／L与（1．3±0．6）mmol／L，均P〈0．053，FPG、FPI、HOMA—IR、收缩压水平亦明显升高（均P〈0．05）。线性相关分析表明TG水平和体质指数（BMI）、FPG、HOMA—IR、TC、收缩压呈正相关（r值分别为0．363、0．392、0．387、0．287、0．268，均P〈0．05）。多元线性回归分析结果亦显示，FPG和HOMA—IR是影响TG水平的独立相关因素（b=0．244，6=0．082，均P〈0．05）。结论高TG血症可能在胰岛素抵抗发生中起重要作用。

Objective To study the changes of circulating triglyceride （TG） in the obese elderly, and to investigate the effect of hypertriglyceridemia on the development of insulin resistance. Methods A total of 82 subjects were divided into simple obesity group, obesity with IGT group, obesity with T2DM group and normal control group. The body height, body weight, blood pressure, fasting plasma glucose （FPG） and insulin （FPI）, circulating TG and total cholesterol （TC） were measured. The homeostasis model assessment-insulin resistance （HOMA-IR） was calculated. Results The levels of serum TG were significantly higher in the simple obesity group （ 1.3 ＋ 0.6） mmol/L, obesity with IGT group （1.9＋ 0.9） mmol/L and obesity with T2DM group （2. 1＋0.7） mmol/L than in the normal controls （（1.0＋0.2）retool/L, all P〈0. 051. Furthermore, the levels of TG, FPG, FPI, HOMA-IR and systolic pressure were significantly higher（all P〈0.05） in obesity with IGT group and obesity with T2DM group than in simple obesity group. There were significantly positive correlations between TG and body mass index （BMI）, FPG, HOMA-IR, TC, systolic pressure respectively （all P〈 0.05）. Multiple linear regression analysis indicated that FPG and HOMA-IR were the independent factors affecting TG （both P 〈 0.05 ）. Conclusions Hypertriglyceridemia may play an important role in the development of insulin resistance.