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作 者:杨晓洁[1] 姚晓红[1] 严款[1] 黄千[1] 周智广[1] 陈妙娇[1] 伍贤平[1] 刘石平[1]
机构地区:[1]中南大学湘雅二医院糖尿病中心内分泌科内分泌研究所,长沙410011
出 处:《中华医学杂志》2013年第36期2867-2870,共4页National Medical Journal of China
摘 要:目的探讨成人体脂分布与胰岛素抵抗、胰岛β细胞功能及代谢紊乱的关系。方法纳入2012年2—11月在中南大学湘雅二医院的成年体检人群共174例,采集人体学参数,进行口服葡萄糖耐量试验(OGTT)、胰岛素释放试验(IRT)并检测血生化指标,采用双能X线吸收法(DEXA)测量体脂分布。结果受试者的躯干/全身脂肪比(T/B)、腰/臀部脂肪比(A/G)与血压、血脂、血糖、稳态模型胰岛素抵抗指数(HOMA。IR)、高敏C反应蛋白(hs—CRP)呈正相关。与代谢正常组比较,代谢紊乱组的体质指数(BMI)、腰围、腰臀比、腰围/身高比(WHtR)、T/B、A/G均高(均P〈0.05)。多元逐步回归分析显示,lnHOMA—IR的主要影响因素为BMI(B=0.36,P=0.000)和T/B(p=0.19,P=0.033);稳态模型胰岛β细胞的自然对数(1nHOMA—β)的主要影响因素为臀部脂肪含量(B=0.31,P=0.000)。Logistic回归分析提示,腰部脂肪含量增加(OR=3.01,95%CI1.86—8.17)和A/G增加(OR=2.71,95%CI1.75—6.56)分别是发生高血糖、血脂异常的危险因素。结论躯干及腰部脂肪含量增加可促进胰岛素抵抗、代谢紊乱。躯干及臀部脂肪含量分别是胰岛素抵抗、胰岛β细胞功能的主要影响因素。腰部脂肪含量是糖脂代谢异常的主要危险因素。Objective To explore the relationship between body fat distribution, insulin resistance, islet β cell function and metabolic disorders in adult population. Methods From February to November 2012, a total of 174 subjects aged 20 -68 years were recruited. Their anthropometric parameters, blood biochemical indices and the results of oral glucose tolerance test (OGTF) and insulin releasing test (IRT) were collected. Body fat distribution was measured with dual energy X-ray absorptiometry (DEXA). Results The values of trunk/total fat mass (T/B) and android/gynoid fat mass ratio (A/G) were positively correlated with blood pressure, blood lipid, plasma glucose, insulin resistance index (HOMA-IR) and high- sensitivity C-reactive protein. Compared with the group of normal metabolism, the group of metabolic disorders had higher T/B and A/G ( P 〈 0. 05 ) . After multiple stepwise regression analysis, the main influencing factors of lnHOMA-IR and lnHOMA-β were T/B and G respectively. Logistic regression showed that A (OR=3.01, 95%CI 1.86 -8.17) was a risk factor for diabetes and A/G (OR =2.71, 95%CI 1.75- 6. 56 ) a risk factor for dyslipidemia. Conclusions Trunk and android fat deposition aggravates insulin resistance, metabolic disorders. And the main influencing factors of insulin resistance and islet β cell function are trunk and gynoid fat respectively. Android fat mass is a major risk factor for glycolipid metabolism.
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