论文部分内容阅读
目的探讨体脂分布特点与代谢综合征(MS)、颈动脉内膜中层厚度(IMT)及尿白蛋白排泄率(UAER)的关系。方法2006-2008年于我院行健康体检者182例为研究对象,未经降血糖、降血脂、利尿、降压、抗尿酸药物治疗。在脐水平测定腰围和CT测定内脏脂肪面积及体脂分布,多普勒超声心动仪测量颈动脉IMT,散射比浊法测定UAER。将研究对象分组为内脏型肥胖组[腰围≥90(男)或≥85cm(女),内脏脂肪面积≥100cm2,n=71)、皮下型肥胖组[腰围≥90(男)或≥85cm(女),内脏脂肪面积<100cm2,n=80]及正常对照组[腰围<90(男)或<85cm(女),n=31]。结果内脏型肥胖组MS发生率高于皮下型肥胖组(63.7%比31.9%,P<0.01)。内脏型肥胖组IMT高于皮下型肥胖组[(0.95±0.14)比(0.77±0.12)mm,P<0.05]与正常对照组[(0.71±0.13)mm,P<0.05]。内脏型肥胖组UAER高于皮下型肥胖组[(31.05±19.87)比(22.75±9.32)mg/24h,P<0.01]与正常对照组[(9.95±6.23)mg/24h,P<0.01]。皮下型肥胖组UAER高于正常对照组(P<0.05)。Spearman秩相关分析显示内脏脂肪蓄积随代谢综合征组分增加而增加(r=0.65,P<0.01)。Pearson直线相关分析显示内脏脂肪蓄积与IMT、UAER呈正相关(r=0.59,P<0.01;r=0.61,P<0.01);皮下脂肪蓄积与UAER呈正相关(r=0.53,P<0.05)。多元逐步线性回归分析显示内脏脂肪面积、高密度脂蛋白胆固醇(HDL-C)、收缩压及低密度脂蛋白胆固醇可用作IMT的解释变量;内脏脂肪面积、空腹血糖及HDL-C可作为UAER的解释变量。结论内脏型肥胖MS发生率高于皮下型肥胖,颈动脉IMT主要受内脏脂肪蓄积影响,UAER既受内脏脂肪影响也受皮下脂肪影响。
Objective To explore the relationship between body fat distribution and metabolic syndrome (MS), carotid artery intima-media thickness (IMT) and urinary albumin excretion rate (UAER). Methods A total of 182 cases of physical examination in our hospital from 2006 to 2008 were selected as research objects without hypoglycemic, hypolipidemic, diuretic, antihypertensive and anti-uric acid drugs. Measurements of visceral fat area and body fat distribution at the umbilical level were performed on the waist circumference and CT. The carotid IMT was measured by Doppler echocardiography and the UAER was measured by nephelometry. Subjects were grouped into visceral obesity group [waist circumference ≥90 (male) or ≥85 cm (female), visceral fat area ≥100 cm 2, n = 71), subcutaneous obesity group ), Visceral fat area <100 cm2, n = 80] and normal controls [waist circumference <90 (male) or <85 cm (female), n = 31]. Results The incidence of MS in visceral obesity group was higher than that in subcutaneous obesity group (63.7% vs. 31.9%, P <0.01). The IMT in visceral obesity group was significantly higher than that in subcutaneous obesity group [(0.95 ± 0.14) vs (0.77 ± 0.12) mm, P <0.05] compared with the control group [(0.71 ± 0.13) mm, P <0.05]. The percentage of UAER in visceral obesity group was significantly higher than that in subcutaneous obesity group [(31.05 ± 19.87) vs (22.75 ± 9.32) mg / 24h, P <0.01] compared with that in control group [(9.95 ± 6.23) mg / 24h, P <0.01. UAER in subcutaneous obesity group was higher than that in normal control group (P <0.05). Spearman rank correlation analysis showed that visceral fat accumulation increased with the increase of metabolic syndrome components (r = 0.65, P <0.01). Pearson linear correlation analysis showed that there was a positive correlation between visceral fat accumulation and IMT, UAER (r = 0.59, P <0.01; r = 0.61, P <0.01), and subcutaneous fat accumulation positively correlated with UAER (r = 0.53, P <0.05). Multivariate stepwise linear regression analysis showed that visceral fat area, high density lipoprotein cholesterol (HDL-C), systolic blood pressure and low density lipoprotein cholesterol can be used as explanatory variables of IMT; visceral fat area, fasting blood glucose and HDL-C can be used as UAER Explanatory variables. Conclusion The incidence of visceral obesity MS is higher than that of subcutaneous obesity. The carotid artery IMT is mainly affected by visceral fat accumulation. UAER is also affected by visceral fat and subcutaneous fat.