Objective To investigate the distribution of CXCL5 gene promoter - 156G/C polymorphism in obesity patients with type 2 diabetes mellitus ( T2DM ) and its relationship with T2DM. Methods 210 T2DM patients ( T2DM group ) admitted to the endocrinology department of our hospital from February to October in 2009 and 171 healthy people ( control group ) underwent physical examination in the same period were involved into the study. PCR - RFLP method was used to detect the polymorphism of CXCL5 gene promoter region - 156G/C in the two groups, and the height, body weight and BMI were also detected. The T2DM group and control group were further divided into non -obesity T2DM group, obesity T2DM group, non -obesity control group and obesity control group by taking BMI ≥25 kg/m2 as criteria. The genotype distribution of CXCL5 gene promoter region - 156G/C and allele frequency of the four groups were compared. Results The genotype distribution and allele frequency of CXCL5 gene promoter region - 156G/C between T2DM group and control group showed no statistically significant difference ( P> 0. 05 ), but there were statistically significant differences among the four sub - groups ( P < 0. 05 ), and there were statistically significant differences among the four sub - groups pairwise between non - obesity T2DM group and non - obesity T2DM group, obesity T2DM group and non - obesity control group, obesity control group and non - obesity control group, obesity control group and non - obesity T2DM group ( P <0. 05 ), but there was no statistically significant difference between obesity T2DM group and obesity control group and between obesity T2DM group and non - obesity control group ( P > 0. 05 ) . Conclusion The distribution of CXCL5 promoter gene - 156G/C polymorphism may relate to obesity, but may not a risk factor for T2DM. The mutation of CXCL5 promoter gene - 156G/C may play an important role in obesity.%目的 探讨肥胖2型糖尿病(T2DM)患者趋化因子CXCL5基因启动子-156位点G/C多态性分布及其与肥胖T2DM的关系.方法 选取2009年2-10月在我院内分泌科住院的T2DM患者210例(T2DM组)及同期在我院体检的健康者171例(对照组),应用聚合酶链反应限制性片段长度多态性(PCR-RFLP)技术检测两组受检者外周血趋化因子CXCL5基因启动子-156位点G/C多态性,并测量受检者的身高、体质量,计算体质指数(BMI).以BMI≥25 kg/m2为肥胖标准将T2DM组及对照组分为非肥胖T2DM组、肥胖T2DM组、非肥胖对照组、肥胖对照组,比较各亚组CXCL5基因启动子-156位点基因型分布及等位基因频率.结果 T2DM组及对照组受检者趋化因子CXCL5基因启动子-156G/C位点基因型分布及等位基因频率比较,差异无统计学意义(P＞0.05);而4个亚组间-156G/C位点基因型分布及等位基因频率比较,差异有统计学意义(P＜0.05).-156G/C位点基因型分布及等位基因频率组间两两比较,如肥胖T2DM组与非肥胖T2DM组、非肥胖对照组比较,肥胖对照组与非肥胖对照组、非肥胖T2DM组比较,差异均有统计学意义(P＜0.05);而肥胖T2DM组与肥胖对照组比较,非肥胖T2DM组与非肥胖对照组比较,差异均无统计学意义(P＞0.05).结论 趋化因子CXCL5基因启动子-156位点G/C多态性与肥胖有关,可能不是糖尿病发病的危险因素.该基因启动子-156位点G-C变异有可能是引起肥胖的重要遗传因素.
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