肥胖对糖脂代谢和血压水平影响的分析

Study on the Effect of Obesity on Glucolipid Metabolism and Blood Pressure Level

目的研究肥胖对糖脂代谢及血压的影响,并探讨其病理生理学机制。方法选取2009年4月至2012年3月在南京市大厂医院体检中心进行健康体检的肥胖患者31例作为肥胖组,33例超重患者为超重组,37例健康人作为对照组。分别测定三组研究对象的空腹血糖(FPG)、空腹胰岛素(FINS)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、尿酸(UA)、收缩压(SBP)、舒张压(DBP)、身高及体质量,计算胰岛素抵抗指数(HOMA-IR)、β细胞分泌功能指数(HOMA-β)和体质量指数(BMI),对各组数据进行比较。结果三组研究对象的FPG、FINS、HOMA-IR、UA、TC、TG、HDL-C及SBP、DBP比较,差异有统计学意义(P<0.05),HOMA-β比较差异无统计学意义(P>0.05);肥胖组与超重组的FINS、HOMA-IR、TG、UA均显著高于对照组(P<0.01),HDL-C则显著低于对照组(P<0.01);肥胖组FPG、TC、SBP、DBP显著高于对照组(P<0.05),而超重组的与对照组比较无统计学意义(P>0.05);肥胖组FINS、HOMA-IR、TG、UA显著高于超重组(P<0.05或P<0.01),HDL-C则显著低于超重组(P<0.01),两组FPG、TC、SBP、DBP比较无统计学意义(P>0.05)。结论肥胖可导致胰岛素抵抗,其病理生理机制促进了代谢综合征其他组分,如血糖、血脂及血压的进展。

Objective To investigate the effect of obesity on glucolipid metabolism and blood pressure, as well as its underlying mechanism. Methods A total of 101 cases of patients underwent physical examina- tion in the healthcare center of Nanjing Daehang Hospital from Apr. 2009 to Mar. 2012 were randomly selected,including 31 obese patients as the obesity group,33 over-weight patients as the over-weight group, and 37 health people as the control group. Fasting plasma glucose （ FPG）, fasting insulin （ FINS ）, total cholesterol （ TC ）, triglyceride （ TG）, high density lipoprotein cholesterol （ HDL-C ）, uric acid （ UA ）, systolic blood pressure （SBP）, diastolic blood pressure （DBP）, body height and weight of the three groups were measured, and insulin resistance index（HOMA-IR） ,the function index of islet beta-cell（HOMA-13） and body mass index （BMI） were calculated. ANOVA was applied for the interelass comparison. Results FPG, FINS, HOMAIR, UA,TC, TG, HDL-C, SBP and DBP differed significantly among the three groups, the differences were statistically significant （ P 〈 0.05 ）, but HOMA-13 had no statistically significant difference （ P 〉 0.05 ）. Compared with the control group, FINS, HOMA-IR, TG and UA of the obesity group and over-weight group were significantly higher（P 〈 0. O] ） ,whereas HDL-C was significantly lower than the control group（ P 〈 0.01 ）. FPG,TC ,SBP and DBP of the obesity group were significantly higher than those of the control group（ P 〈 0.05）, while there were no statistically significant differences in those indexes between the over-weight group and the control group. Compared with the over-weight group, FINS, HOMA-IR, TG and UA of the obesity group were significantly higher（ P 〈 0.05 or P 〈 0.01 ）, and HDL-C was significantly lower（ P 〈 0. 01 ） , while there were no statistically significant differences of FPG, TC, SBP and DBP between the two groups （P 〉 0.05）. Conclusion Obesity can cause insulin resistance, its pathophysiological mechanism plays an important role in the development of metabolic syndrome.