University Institute of Biochemistry & Biotechnology, PMAS- Arid Agriculture University Rawalpindi, Rawalpindi, Pakistan.
Department of Biochemistry and Molecular Biology, University of Sialkot, Sialkot, Pakistan.
PLoS One. 2022 Sep 20;17(9):e0274904. doi: 10.1371/journal.pone.0274904. eCollection 2022.
Obesity is highly polygenic disease where several genetic variants have been reportedly associated with obesity in different ethnicities of the world. In the current study, we identified the obesity risk or protective association and BMI raising effect of the minor allele of adiponectin, C1Q and collagen domain containing (ADIPOQ), cholesteryl ester transfer protein (CEPT), FTO alpha-ketoglutarate dependent dioxygenase (FTO), leptin (LEP), and leptin receptor (LEPR) genes in a large cohort stratified into four BMI-based body weight categories i.e., normal weight, lean, over-weight, and obese. Based on selected candidate genetic markers, the genotyping of all study subjects was performed by PCR assays, and genotypes and allele frequencies were calculated. The minor allele frequencies (MAFs) of all genetic markers were computed for total and BMI-based body weight categories and compared with MAFs of global and South Asian (SAS) populations. Genetic associations of variants with obesity risk were calculated and BMI raising effect per copy of the minor allele were estimated. The genetic variants with higher MAFs in obese BMI group were; rs2241766 (G = 0.43), rs17817449 (G = 0.54), rs9939609 (A = 0.51), rs1421085 (C = 0.53), rs1558902 (A = 0.63), and rs1137101 (G = 0.64) respectively. All these variants were significantly associated with obesity (OR = 1.03-4.42) and showed a high BMI raising effect (β = 0.239-0.31 Kg/m2) per copy of the risk allele. In contrast, the MAFs of three variants were higher in lean-normal BMI groups; rs3764261 A = 0.38, rs9941349 T = 0.43, and rs7799039 G = 0.40-0.43). These variants showed obesity protective associations (OR = 0.68-0.76), and a BMI lowering effect per copy of the protective allele (β = -0.103-0.155 Kg/m2). The rs3764261 variant also showed significant and positive association with lean body mass (OR = 2.38, CI = 1.30-4.34). Overall, we report six genetic variants of ADIPOQ, FTO and LEPR genes as obesity-risk markers and a CETP gene variant as lean mass/obesity protective marker in studied Pakistani cohort.
肥胖是一种高度多基因疾病,据报道,几种遗传变异与世界各地不同种族的肥胖有关。在本研究中,我们确定了肥胖风险或保护关联以及脂肪细胞因子(ADIPOQ)、胆固醇酯转移蛋白(CEPT)、FTOα-酮戊二酸依赖性双加氧酶(FTO)、瘦素(LEP)和瘦素受体(LEPR)基因的次要等位基因在根据 BMI 分为四个体重类别(正常体重、瘦、超重和肥胖)的大队列中的 BMI 升高效应。基于选定的候选遗传标记,通过 PCR 分析对所有研究对象进行基因分型,并计算基因型和等位基因频率。计算了所有遗传标记的次要等位基因频率(MAF),并与全球和南亚(SAS)人群的 MAF 进行了比较。计算了变异与肥胖风险的遗传关联,并估计了每个次要等位基因的 BMI 升高效应。在肥胖 BMI 组中,MAF 较高的遗传变异有:rs2241766(G = 0.43)、rs17817449(G = 0.54)、rs9939609(A = 0.51)、rs1421085(C = 0.53)、rs1558902(A = 0.63)和 rs1137101(G = 0.64)。所有这些变异均与肥胖显著相关(OR = 1.03-4.42),且每个风险等位基因的 BMI 升高效应较大(β = 0.239-0.31 Kg/m2)。相比之下,三个变异的 MAF 在瘦正常 BMI 组中较高:rs3764261 A = 0.38、rs9941349 T = 0.43 和 rs7799039 G = 0.40-0.43)。这些变异与肥胖保护关联(OR = 0.68-0.76),并且每个保护等位基因的 BMI 降低效应(β = -0.103-0.155 Kg/m2)。rs3764261 变异也与瘦体重呈显著正相关(OR = 2.38,CI = 1.30-4.34)。总的来说,我们报告了 ADIPOQ、FTO 和 LEPR 基因的六个遗传变异作为肥胖风险标志物,以及 CETP 基因变异作为研究巴基斯坦队列中的瘦体重/肥胖保护标志物。