【摘要】 目的 探讨成都市成华区中老年人群血脂水平、分布特点及其与胰岛素抵抗指数（HOMA-IR）的关系。 方法 2007年5月在此区中老年（50~79岁）人群中随机抽取672人进行心血管危险因素研究调查，对其血脂水平及HOMA-IR进行统计分析。 结果 人群当中①女性各血脂项目的水平均比男性高，其中总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）的差异有统计学意义（P lt;0.05）；②三酰甘油（TG）升高的比例较高，其中男性为30.0%，女性为27.6%；大部分人群HDL-C、低密度脂蛋白胆固醇（LDL-C）水平处于合适范围，HDL-C降低的比例为6.0%，LDL-C升高的比例为7.3%；③随着TG水平的升高、HDL-C 水平的降低，HOMA-IR呈升高趋势；LDL-C水平的升高，HOMA-IR呈升高趋势，仅在女性人群中差异有统计学意义（P lt;0.05），在男性人群中差异无统计学意义；④TG与HOMA-IR呈正相关，相关系数为0.185（P=0.000）；HDL-C与HOMA-IR呈负相关，相关系数为-0.145（P=0.000）。LDL-C与HOMA-IR呈正相关，相关系数为0.099（P=0.010）。 结论 TG增高是成都市成华区中老年人群的显著特点，女性HDL-C比男性高；血脂紊乱与胰岛素抵抗相关。
【Abstract】 Objective To investigate the relationship between blood lipids level and homeostasis model assessment-insulin resistance (HOMA-IR) in elder people in Chengdu. Methods In May 2007, 672 people aged from 50 to 79 years in Chengdu were recruited by random sampling methods for the survey of cardiovascular risk factors. The blood lipids level and HOMA-IR were statistically analyzed. Results ① The serum total cholesterol (TC) and high density lipoprotein chole sterol (HDL-C) were obviously higher in women than those in men (P lt;0.05). ② Triacylglycerol (TG) increased in 30.0% of men and 27.6% of women; HDL-C and low density lipoprotein cholesterin (LDL-C) in most of the involved people were appropriate. ③ HOMA-IR increased as the TG level increased and HDL-C decreased; HOMA-IR increased as the LDL-C level increased, which was significant in the females (P lt;0.05). ④ HDL-C was positively correlated with HOMA-IR (r=-0.145, P=0.000); LDL-C was positively correlated with HOMA-IR (r=0.099, P=0.010). Conclusion The increase of hypertriglyceridemia was the most frequent type of the dislipidemia in the elder people in Chengdu; HDL-C level is higher in women than in men. Dyslipidemia is correlated with insulin resistance.
Citation： CHEN Xiaoni,CHEN Xiaoping,WU Kai,WANG Si,LI Longxin,WAN Liyan. Relationship between Blood Lipids Level and Homeostasis Model Assessment-Insulin Resistance in Elder People in Chengdu. West China Medical Journal, 2011, 26(3): 328-330. doi: Copy