健康人群肿瘤坏死因子-α基因多态性的分析

了解汉族健康人群中TNF-A基因多态性的分布,研究TNF-α表达与相关疾病之间的联系。采用PCR-限制性长度片段多态分析法检测140名重庆地区汉族健康人群的TNF—A-308,TNF—A-857位点基因多态性,计算其基因型和等位基因频率,结果显示TNF-A-308G／G、G／A、4朋基因型的频率分别为89％、11％、1％,其等位基因的发生频率以G等位基因最常见（93％）,其次为A等位基因（7％）。TNF—A-857C／C、C／T、形,基因型的频率分别为68％、36％、8％,其等位基因发生频率以C等位基因最常见（81％）,其次为T等位基因（19％）。由结果可以得出重庆地区汉族健康人群TNF—A-308位点存在G／A多态性,TNF-A-857位点存在C／T多态性。     

儿童单纯肥胖症血清瘦素、脂联素相关性研究及意义

目的:检测单纯肥胖症患儿血清中瘦素、脂联素水平,评价其临床意义.方法:依据儿童单纯肥胖症诊断标准选取40名患儿,男女各20名,选取20名年龄、性别类同的健康儿童作为对照组.应用ELISA法检测患儿血清瘦素及脂联素水平,与健康儿童进行比较及男女两组之间比较.结果:与对照组相比,患儿血清脂联素水平降低,瘦素水平升高,差异有统计学意义(P<0.05),男女两组比较,差异无统计学意义(P>0.05).结论:肥胖症儿童脂联素、瘦素水平的变化与儿童肥胖症发病密切相关,对儿童肥胖症的发展趋势及预后判断有一定意义,脂联素、瘦素素水平是肥胖发生的预测指标.     

脂联素在炎症性疾病中的研究进展

脂肪组织不仅是一个被动的能量储存的器官,它还是一个调节机体内分泌、能量代谢及炎症的内分泌器官.脂联素是由Scherer等于1995年在小鼠3T3-L1前脂肪细胞系的分化过程中分离克隆发现的主要由脂肪细胞分泌的一种内源性生物活性蛋白质.目前的研究表明脂联素具有抑制动脉粥样硬化、保护心血管系统、改善胰岛素抵抗、调节脂质代谢及抗炎等多种功能.现就脂联素的结构、基因表达调控以及它在动脉粥样硬化、心脏疾病、脂质代谢等肥胖引起的慢性炎症性疾病和自身免疫性疾病(如类风湿性关节炎,系统性红斑狼疮,克罗恩病)及急性肝炎等急性炎症性疾病中的作用作一综述.系统地介绍脂联素在各种炎症性疾病中发挥效用的机制,更好地认识脂联素的作用机理,为以后介入脂联素作用的调节过程、开发研究新药物等后续研究打下良好的基础.     

可溶性肿瘤坏死因子受体II-脂联素球部融合蛋白的真核表达及生物学活性检测

本研究设计和构建了一种人肿瘤坏死因子受体II胞外区与人脂联素球部的融合基因sTNFRII-gAD,且相应的融合蛋白在哺乳动物细胞BHK-21S的无血清培养体系中实现了表达,并对该融合蛋白进行了初步鉴定。首先,用RT-PCR方法从人的外周血淋巴细胞总RNA中扩增人肿瘤坏死因子II型受体胞外区基因片段,与脂联素球部基因片段融合,克隆至pAAV2neo表达载体中,构建成pAAV2neo-sTNFRII-gAD。随后,用pAAV2neo-sTNFRII-gAD转染BHK-21S细胞获得G418抗性细胞BHK-21S/pAAV2neo-sTNFRII-gAD;然后,将原来含有血清的培养液换成无血清的化学成分限定的培养液,细胞从贴壁培养方式转换成悬浮培养方式;最后,收集BHK-21S/pAAV2neo-sTNFRII-gAD无血清悬浮培养24h后的培养上清,进行sTNFRII-gAD融合蛋白的鉴定分析。酶切鉴定和测序结果显示,所构建的pAAV2neo-sTNFRII-gAD质粒结构正确,sTNFRII-gAD序列与预期一致;分别用抗人肿瘤坏死因子受体II和抗人脂联素球部的单克隆抗体检测pAAV2neo-sTNFRII-gAD瞬时转染的BHK-21S细胞,免疫荧光呈现阳性;免疫印迹分析在pAAV2neo-sTNFRII-gAD稳定转染的BHK-21S细胞上清中检测到sTNFRII-gAD融合蛋白的表达,并以单体、三聚体和三聚体以上的多聚体形式存在。活性测定结果表明,sTNFRII-gAD融合蛋白具有显著抑制TNFα杀伤L929细胞的活性。因此,本研究为下一步大量制备sTNFRII-gAD融合蛋白用于体内外功能研究提供了良好基础。     

鸭脂联素基因单核苷酸多态性检测及群体遗传分析

以昆山麻鸭、樱桃谷鸭、高邮鸭、荆江麻鸭、金定鸭, 山麻鸭、龙白鸭和白羽番鸭8个鸭品种为实验材料, 根据鸭脂联素基因开放阅读框序列设计5对引物, 用PCR-SSCP方法进行单核苷酸多态性分析,并对不同品种群体进行群体遗传学分析。结果发现引物4扩增片段上共存有7个单碱基突变, 第430、457、523处的G-A 、A-G、T-C单碱基突变导致第144、153、175个氨基酸分别由丙氨酸（A）变为苏氨酸（T）、异亮氨酸（I）变为缬氨酸(V)、酪氨酸(Y)变为组氨酸(H); 而C507T, T540C, C576T和C597T 4个单碱基突变为沉默突变。鸭群中表现出AA、AB、AC、BB、BC、CC、DD、DE 8种基因型。8种基因型在8个鸭品种间分布存在极显著的差异(P<0.01)。除金定鸭外, 其他品种均处于Hardy-Weinberg平衡状态。群体遗传分析表明金定鸭的纯合度最高, 高邮鸭最低, 其他各群体的纯合度较相近; 金定鸭为低度多态, 高邮鸭为高度多态, 其他品种为中度多态。表明鸭脂联素基因不同品种中具有丰富的单核苷酸多态性, 可以进一步作为候选基因来分析其与脂肪性状的相关性。     

肥胖儿童血浆脂联素的变化及临床意义

目的:检测儿童血浆脂联素(ADPN)的变化及其与肥胖的关系,探讨ADPN在儿童肥胖症发病的意义.方法:265名儿童随机分为肥胖组和正常对照组,分别测定腰围(WC),臀围,腰臀比(WHR),体脂百分比(%BF),甘油三酯(TG),总胆固醇(TC),高密度脂蛋白胆固醇(HDL-C),低密度脂蛋白胆固醇(LDL-C),空腹血糖(FBG),空腹胰岛素(FINS)及ADPN,计算稳态模型胰岛素抵抗指数(HOMA-IR),并分析ADPN与体质量指标、糖脂代谢指标的关系.结果:肥胖组儿童ADPN水平低于正常组儿童(P＜0.05),且与BMI、WHR、HOMA-IR、%BF、FINS、TG呈显著负相关(P均＜0.05);多元逐步回归分析显示%BF、BMI、HOMA-IR、FINS是影响ADPN的主要因素.结论:肥胖儿童ADPN水平显著下降,且与体脂含量及胰岛素抵抗密切相关.     

肿瘤坏死因子-α与心脏疾病

肿瘤坏死因子-α是一种具有多种生物学效应的细胞因子。新近研究表明,TNF-α参与冠心病、心肌炎、心力衰竭等多种心脏疾病的发生和发展过程,并可能介导了心脏手术后的炎症反应。如何抑制病理条件下高浓度血清TNF-α对机体造成的损害成为当前人们关注的课题。     

白介素-1和肿瘤坏死因子-α基因多态性与幽门螺杆菌相关性胃十二指肠疾病的关系

目的探讨汉族人群中IL-1和TNF-α基因多态性与H.pylori相关性胃十二指肠疾病之间的关系。方法选取H.pylori阳性的142例胃十二指肠疾病患者和140例健康对照者,采用PCR-限制性长度片段多态方法检测该人群中IL-1B-511、TNF-A-308、TNF-A-857位点多态性和IL-1受体拮抗剂基因的多态性。结果 IL-1B-511和IL-1RN各基因型的频率在疾病组和对照组中的分布差异无统计学意义。在疾病组中TNF-A-308和TNF-A-857各基因型的频率与对照组比较,分布有差异,具有统计学意义(P0.05)。经Logistic回归分析,与携带TNF-A-308G/G者比较,携带TNF-A-308 A/A者发生胃十二指肠疾病的危险性为OR=15.37(95%CI:3.50-67.50);携带TNF-A-308 A/G者发生胃十二指肠疾病的危险性为OR=5.12(95%CI:2.54-10.34);与携带TNF-A-857 C/C者相比较,携带TNF-A-857 T/T者发生胃十二指肠疾病的危险性为OR=3.20(95%CI:1.35-7.60)。结论 IL-1B-511和IL-1RN各基因型与幽门螺杆菌相关性胃十二指肠疾病的发生不相关。TNF-α基因多态性与幽门螺杆菌相关性胃十二指肠疾病的发生相关。     

中国人群中肿瘤坏死因子α-308 A/G基因多态和α2-巨球蛋白基因缺失多态与晚发性阿尔茨海默病无相关性

晚发性阿尔茨海默病 (LOAD)是老年痴呆中最常见的一种 ,它是一种病因复杂、由遗传因素和环境等其他因素共同作用引起的老年期疾病。服用非甾类抗炎类药物能延缓或防止LOAD的发病说明炎症反应可能参与LOAD病理 ,肿瘤坏死因子 (TNF)是炎症反应中主要的细胞因子 ,并且能增加 β 淀粉样肽 (Aβ)的产生说明其可能是LOAD的易感基因。α2 巨球蛋白 (A2M)是一种血清蛋白酶抑制剂 ,它是低密度脂蛋白受体相关蛋白 (LRP)主要的配体 ,并且能与Aβ结合并介导其降解和清除 ,说明它可能是另一个LOAD的易感基因。在 6 7名晚发性阿尔茨海默病人和 14 2名正常对照中比较了载脂蛋白E基因 (APOE)、TNF启动子区 (- 30 8A G)多态和A2M一 5bp核苷酸缺失 (I D)多态 (A2M 2 )与LOAD发病风险的关系。结果显示 ,APOEε4等位基因在AD病人组中显著高于对照组 (χ2=11 6 6 ,P <0 0 1) ,而TNF(- 30 8A G)多态和A2M缺失多态的基因型和等位基因在LOAD病人组和对照组中都无显著差别 (P >0 1)。按年龄和APOEε4等位基因分组同样无相关性 ,说明TNF 30 8A G位点的多态与A2M缺失不是中国人群的晚发性老年痴呆的风险因子     

脂联素基因单核苷酸多态性与Ⅱ型糖尿病合并肥胖及胰岛素抵抗相关联

脂联素是近年新发现的脂肪组织特异性的细胞因子,其mRNA是脂肪组织中含量最丰富的基因转录产物,该因子可通过多种途径影响个体对胰岛素的敏感性。脂联素基因多态性与肥胖、胰岛素抵抗和2型糖尿病密切相关,而与冠心病相关性研究的报道较少。本研究以中国汉族人群1,098例为对象,其中304例冠心病(CHD)患者,389例糖尿病患者(T2DM),及405例性别年龄相匹配的正常对照,采用PCR-RFLP技术对脂联素基因-4522C/T进行基因分型,并分别对血脂水平、胰岛素抵抗、体重指数等临床数据进行分析比较。研究结果显示,脂联素基因-4522C/T各基因型及等位基因在CHD组与对照组、T2DM组与对照组中的分布差异无显著性;经分组分析发现,T2DM合并肥胖患者BMI≥25kg/m2TT基因型及T等位基因明显多于对照组,差异有显著性,P=0.014和P=0.034;TT基因型T2DM患者胰岛素抵抗指数(HOMA-IR)显著高于携带有C等位基因的T2DM患者,P=0.0069。本研究提示脂联素基因-4522C/T与中国汉族人群T2DM合并肥胖的发生及T2DM患者胰岛素抵抗相关,是引发糖尿病患者肥胖和胰岛素抵抗的重要候选基因,而与冠心病的发生无关联。     

Single nucleotide polymorphisms within the promoter region of the rhesus monkey tumor necrosis factor-alpha gene

The human TNF-alpha gene is characterized by several single nucleotide polymorphisms (SNPs) in its promoter region, in part having been shown to influence TNF-alpha expression and susceptibility to various diseases. The rhesus macaque is widely used as an animal model for a variety of TNF-alpha associated pathological conditions, but little is known about genetic variation within the TNF-alpha promoter region. In order to check for such polymorphisms, primers based on rhesus sequence within 5 UTR were designed and used to amplify a 1 kb product from genomic DNA of 29 animals. Sequencing and cloning revealed a total of 11 polymorphisms leading to five different haplotypes.     

The rs9939609 polymorphism in the fat mass and obesity associated (FTO) gene is associated with obesity in Tunisian population

Abstract

Context: Variations in the fat mass and obesity-associated gene (FTO) has been associated with obesity in many populations, but the results are conflicting.

Objective: The aim of this study was to evaluate the effect of the rs9939609 polymorphism in the FTO gene on obesity risk and plasma leptin, adiponectin, insulin and lipid concentrations in Tunisians.

Materials and methods: Four hundred and ninety-four subjects with obesity and 334 non-obese participated in this study. The rs9939609 (T/A) genotype was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.

Results: Significant differences in genotype frequencies were observed between cases and controls. In the separate analysis by gender, the association between the AA genotype and obesity was statistically significant in women but not in men. After stratification by obesity class this association remains only with obesity class III.

Discussion: Our study is in agreement with studies on Caucasian, Portuguese and Cebu Filipino populations where a gender-specific association was found between rs9939609 polymorphism and obesity. It is also in agreement with studies on Mexican, Spanish and European populations, where an association was found with obesity class III.

Conclusion: The rs9939609 polymorphism of FTO gene is associated with obesity, especially obesity class III in women.     

The association of IL-8-251T/A polymorphism with complicated malaria in Karbi Anglong district of Assam

Amongst host genetic factors, cytokine gene polymorphism can be anticipated to be an important factor as qualitative, quantitative and time of secretion play an important role in disease outcome. We have investigated association of cytokine promoter SNPs with risk of Plasmodium falciparum malaria and disease severity in a case control study in malaria endemic Karbi Anglong district of Assam, India.Frequency of IL-8-251T/A (p = 0.03 and p = 0.01) and TGF-β1-509C/T (p = 0.02 and p = 0.03) was higher in malaria in comparison to control participants and non-malarial fever controls. Interestingly, a higher frequency of mutant allele of IL-10-819T/C was observed in non-malarial fever controls compared to malaria thus suggesting its role as a distinguishing marker of the two disease groups. Higher IL-8 expression and increased frequency of IL-8-251T/A in complicated malaria (p = 0.002) was reported indicating its role in susceptibility to complicated malaria.In conclusion, our study suggests the role of mutant genotype of IL-8-251T/A as a marker of complicated malaria in our population. Surprisingly, decreased expression of TGF-β1 in uncomplicated malaria even in presence of high expressing mutant genotype was observed and needs to be investigated in context of the pool of activated cells producing the cytokine.     

Localization of tumor necrosis factor in the canine testis, epididymis and spermatozoa

Tumor necrosis factor (TNF), formerly known as Tumor necrosis factor alpha is now regarded as a natural component of the mammalian seminal plasma (SP). Although not completely clarified, its functions in the SP have been associated with paradoxal roles, such as sperm survival in the female genital tract, while at high levels negatively affect sperm survival and fertility potential. Recently, it has been discovered that canine inseminated spermatozoa display a strong immunoreaction for TNF when lining the female endometrium. As a continuation of this finding, the present work aimed at documenting TNF localization in the canine testes and epididymis and in freshly ejaculated spermatozoa (SPZ) through immunohisto- or cytochemistry.Immunoreaction for TNF was found in all samples used. In the dog testis, TNF immunoexpression was limited to the seminiferous tubules, where late round spermatids (SPD) showed weak intensity of immunostaining, while elongating and elongated SPD evidenced moderate and the residual bodies a strong intensity. In the epididymis, a gradual progressive increase of TNF immunolabelling was found throughout the epididymal regions, ranging from a weak intensity at the caput epididymis to a moderate intensity at the cauda. TNF immunolabelling was found in mature SPZ during the epididymal transit and also in freshly ejaculated SPZ, which showed a strong midpiece immunolabelling. Data presented here provide important information on expression of TNF in spermatozoa, which is acquired by the SPZ during their formation at the testis. It further provides the basis for subsequent studies on the physiological importance of cytokines in sperm function.     

Identification of polymorphism and association analysis with reproductive traits in the porcine RNF4 gene

The ring finger protein 4 gene (RNF4), which might play a role in fetal germ cell development as well as in oocyte and granulosa cell maturation, was one of the potential candidate genes for reproductive traits. In the present work, we isolated the complete coding sequence of porcine RNF4 gene, identified a single nucleotide polymorphism (SNP: T/C) in intron5, and developed a PCR-SacII-RFLP genotyping assay. Association of this SNP with reproductive traits was assessed in three populations with diverse genetic backgrounds. One was Chinese Qingping sows. Another was consisted of crossbred sows derived from Landrace, Large White, Chinese Tongcheng and/or Chinese Meishan (Line DIV). The third is Large White × Meishan (LW × M) F₂ slaughtered population. Statistical analysis demonstrated that, in the first parity, the difference between RNF4 genotypes and reproductive traits of both Qingping and Line DIV sows was not significant. In the second and subsequent litters, CC animals in Qingping population had more piglets born (+1.74 piglets) and piglets born alive (+2.02 piglets) than sows with the TT genotype (P < 0.05). Line DIV sows inheriting the CC genotype had additional 0.69 piglets born compared to the TC animals (P < 0.05) in second and subsequent litters. No significant difference was observed between genotypes and reproductive tracts components in F₂ animals. In addition, we found RNF4 gene has a significant additive effect on both piglet born and piglet born alive in Qingping animals (P < 0.05). Results here suggested that the RNF4 SNP was significantly associated with litter size in two populations and could be useful in selection for increasing litter size in pigs. Further studies were needed to confirm these preliminary researches.     

Leptin and leptin receptor gene polymorphisms and their association with plasma leptin levels and obesity in a multi-ethnic Malaysian suburban population

Background

This study was to investigate the prevalence of single nucleotide polymorphisms (SNPs) in leptin gene LEP (A19G and G2548A) and leptin receptor gene LEPR (K109R and Q223R) and their association with fasting plasma leptin level (PLL) and obesity in a Malaysian suburban population in Kampar, Perak.

Methods

Convenience sampling was performed with informed consents, and the study sample was drawn from patients who were patrons of the Kampar Health Clinic. A total of 408 subjects (mean age, 52.4 ± 13.7 years; 169 men, 239 women; 190 obese, 218 non-obese; 148 Malays, 177 ethnic Chinese, 83 ethnic Indians) participated. Socio-demographic data and anthropometric measurements were taken, and genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).

Results

The LEP A19G, G2548A and LEPR K109R, Q223R variant allele frequencies were 0.74, 0.67 and 0.61, 0.79, respectively. The genotype and allele distributions of these gene variants were significantly different among ethnic groups, but not among body mass index (BMI) classes. Subjects with LEPR K109 and Q223 allele had significantly higher systolic blood pressure and adiposity indices after adjustment for ethnicity (higher BMI, total body and subcutaneous fat; lower skeletal muscle percentage). Subjects with LEPR 109R allele had lower PLL than their wild-type allele counterparts. The influence of LEP A19G and G2548A SNPs on blood pressures, anthropometrics, and PLL was not evident. Interestingly, synergistic effect of the LEP and LEPR SNPs was observed as subjects homozygous for all four SNPs studied exhibited significantly higher subcutaneous fat and PLL than those with other genotype combinations.

Conclusions

The LEP and LEPR SNPs in this study may not be an obesity marker among Malaysians in this population, but were associated with ethnicity. Our findings suggest that each of these SNPs contributes to minor but significant variation in obesity-related traits and in combination they display synergistic effects on subcutaneous fat and PLL.     

The potential biological and clinical significance of the soluble tumor necrosis factor receptors

The role of TNF receptors (TNF-Rs) is not limited to signal transduction but includes extracellular regulatory functions affecting systemic TNF bioavailability. This review summarizes the regulation of TNF-R shedding and its kinetics, the complex interaction between the soluble receptors and their ligand in vitro and in vivo, and the potential diagnostic, prognostic and therapeutic value of the soluble receptors in malignant, inflammatory, infectious and autoimmune disorders.     

Globular adiponectin decreases leptin-induced tumor necrosis factor-alpha expression by murine macrophages: involvement of cAMP-PKA and MAPK pathways

Several lines of evidence have supported a link between obesity and inflammation. The present study investigated the capacity of leptin and globular adiponectin to affect tumor necrosis factor alpha (TNF-alpha) production in murine peritoneal macrophages. Leptin stimulated TNF-alpha production at mRNA as well as protein levels in a dose- and time-dependent manner. Intracellular cAMP concentration was increased and protein kinase A (PKA) was activated with the treatment of leptin, subsequently downstream MAPK signal proteins, ERK1/2 and p38, were phosphorylated. Specific inhibitors for the signal proteins, Rp cAMPS, H89, PD98059, and U0126, or SB203580, suppressed the signaling pathway and TNF-alpha expression. Although gAd partially increased cAMP concentration and PKA activity, it directly reduced leptin-induced ERK1/2 and p38 MAPK phosphorylation thus inhibiting TNF-alpha production. In conclusion, leptin promotes inflammation by stimulating TNF-alpha production, which is mediated by cAMP-PKA-ERK1/2 and p38 MAPK pathways. gAd inhibited leptin-induced TNF-alpha production through suppressing phosphorylation of ERK1/2 and p38 pathways.     

Erythropoietin-dependent autocrine secretion of tumor necrosis factor-alpha in hematopoietic cells modulates proliferation via MAP kinase--ERK-1/2 and does not require tyrosine docking sites in the EPO receptor

Primary erythroid cells and erythroid cell lines may synthesize and secrete tumor necrosis factor-alpha (TNF-alpha) following stimulation with erythropoietin (EPO). The effect of triggering TNF-alpha synthesis and secretion was investigated in erythroleukemia and myeloid cell lines: HCD57, DA3-EPOR, and BAF3-EPOR. The EPO-induced, membrane-bound form of autocrine TNF-alpha seemed to enhance proliferation of HCD57 and DA3-EPOR cells; however, the concentration of secreted autocrine/paracrine TNF-alpha was never sufficient to have an effect. Autocrine TNF-alpha acts through TNFRII receptors to stimulate proliferation. Modulation of mitogen-activated protein kinase (MAPK)/extracellular signal-related kinase (ERK-1/2) activity by the membrane-bound form of autocrine TNF-alpha apparently played a central role in the control of EPO-dependent proliferation of HCD57 and DA3-EPOR cells. Primary erythroid cells and DA3-EPOR cells were found to express similar, high levels of both TNFRI and TNFRII, showing that differential expression of TNF-alpha receptors does not explain why primary cells are inhibited and DA3-EPOR cells are stimulated by autocrine TNF-alpha. BAF3 cells expressing a mutant EPOR with no cytoplasmic tyrosine residues were capable of triggering EPO-dependent TNF-alpha synthesis and secretion, indicating that tyrosine-docking sites in the EPOR were not required for EPO-dependent TNF-alpha secretion.     

Gender specific effect of LIPC C‐514T polymorphism on obesity and relationship with plasma lipid levels in Chinese children

Hepatic lipase (LIPC) is a key rate‐limiting enzyme in lipoprotein catabolism pathways involved in the development of obesity. The C‐514T polymorphism in the promoter region is associated with decreased LIPC activity. We performed a case‐controlled study (850 obese children and 2119 controls) and evaluated the association between LIPC C‐514T polymorphism, obesity and plasma lipid profile in Chinese children and adolescents. Additionally, we conducted a meta‐analysis of all results from published studies as well as our own data. A significant association between the polymorphism and obesity is observed in boys (P = 0.042), but not in girls. And we observed a significant relationship of the polymorphism with total cholesterol (TC) and high density lipoprotein cholesterol (HDL‐C) independent of obesity in boys. The T allele carriers have higher levels of low density lipoprotein cholesterol (LDL‐C) in obese boys, and triglyceride (TG), TC and LDL‐C in non‐obese girls (all P < 0.05). In the meta‐analysis, under dominant model the T allele increased body mass index (BMI) level in boys, while it decreased BMI in girls, and increased the levels of TC both in the overall and subgroups, TG and HDL‐C in the overall and boys, and LDL‐C in the overall (all P < 0.05). Our results suggest that the T allele might carry an increased risk of obesity in Chinese boys. The meta‐analysis suggests that T allele acts as a risk allele for higher BMI levels in male childhood, while it is a protective allele in female childhood. And the polymorphism is associated with the levels of plasma lipids, which may be modulated by obesity and gender.