脂联素基因多态性与肥胖、血清脂联素水平的相关性

目的：研究发现，脂肪组织分泌的脂联素在体脂变化，糖、脂代谢以及抗动脉粥样硬化中发挥有益的作用。分析脂联素基因（apMl）多态性与肥胖、血清脂联素水平的相关性。方法：（1）试验对象：选取2000-08／2003-07在上海市华阳社区肥胖流行病学调查所诊断的超重，月巴胖人群以及上海市第六人民医院门诊就诊的390名患者。男171例，女219例，平均年龄（51±1）岁。纳入标准：①符合世界卫生组织（WHO）肥胖诊断标准。②所有纳入对象均为汉族人。③对试验目的知情同意。（2）试验方法及评估：根据世界卫生组织（WHO）肥胖诊断标准将受试对象分为正常体质量组（体质量指数〈25kg／m^2）182例和超重，月巴胖组（≥25kg／m^2）208例。进一步根据腹腔内脂肪面积将超重，月巴胖组分为腹内型肥胖（腹腔内脂肪面积≥100cm^2）114例和非腹内型肥胖（腹腔内脂肪面积〈100cm^2）94例。采用多聚酶链反应一限制性片段长度多态性方法检测apM1基因第二外显子＋45（Exon2＋45）和第三外显子＋331（Exon3＋331）2个位点的基因多态性。应用核磁共振测定局部体脂，放射免疫分析法测定空腹血清脂联素水平。试验对数据先进行正态分布检验，如果符合正态分布，两组间计量资料的比较采用t检验，多组间比较用啦验。计算基因多态性的基因型频率，确认符合Hardy-Weinberg平衡，计算等位基因频率，基因型分布作Hardy-Weinberg吻合度检验。等位基因频率和基因型频率的比较采用x。检验。结果：正常对照组182例和超重，月巴胖组208例均进入结果分析。①中国汉族人apMl基因Exon2＋45位点存在基因多态性，有3种基因型，即TT，TG，GG；Exon3＋331位点不存在基因多态性，均为TT基因型。②apMl基因Exon2＋45位点基因型及等位基因频率在超重，月巴胖者与正常体质量者之间无?

Association of adiponectin gene polymorphism with obesity and adiponectin

AIM： Studies have suggested that adipose tissue-secreted adiponectin plays a positive rule in body fat alternation, glucose and lipid metabolism and anti-artherusclerusis. This study explored the correlation of adiponectin gene （apM1） polymorphism with obesity and serum adiponectin concentration.
METHODS： ①Between August 2000 and July 2003, 390 overweight/obesity patients （171 males and 219 females） were selected from Huayang community of Shanghai and the Outpatients of Shanghai Sixth People＇s Hospital. All the subjects were Han people with an average age of （51±1） years. They were diagnosed according to the diagnostic criteria for obesity of world health organization （WHO） and participated in the study voluntarily. ②The subjects were divided into two groups according to the diagnostic criteria for obesity of WHO： normal body mass group [n=182, body mass index （BMI） 〈 25 kg/m^2] and overweight/obesity group （n=208, BMI≥25 kg/m^2）. The overweight/obesity subjects were further divided into two groups based on the visceral adipose area （VA）： VA obesity group （n =114, VA≥100 cm^2） and non-VA obesity group （n=94, VA 〈100 cm^2）. The polymorphism apMl at nucleotide ＋45 in exon2 region and that at nucleotide ＋331 in exon3 region were detected with polymerase chain reaction-restriction fragment length polymorphism analysis （PCR-RFLP）. Regional body fat was measured by Magnetic Resonance Imaging. Fasting serum adiponectin concentration was assayed by radioimmunoassay. The data were firstly processed with normal distribution test. If the data were accorded with the normal distribution, the mean of the measurement data between two groups were compared with the t test, and the F test was applied in the comparison among many groups. The genotypic frequency of gene polymorphism was calculated to identify whether it was accorded with Hardy-Weinberg balance, and then the allele frequency was also calculated. The Hardy-Weinberg test was applied to the genotypic d