{"title":"PPARγ Pro12Ala and C161T polymorphisms, but not PPARα L162V, are associated with osteoporosis risk in Turkish postmenopausal women","authors":"Özlem Kurt Şirin, H. Aydogan, M. Uyar, A. Can","doi":"10.26650/ISTANBULJPHARM.2019.18005","DOIUrl":null,"url":null,"abstract":"DOI : 10.26650/IstanbulJPharm.2019.18005 Stimulation of peroxisome proliferator-activated receptors (PPARs) causes mesenchymal stem cells of the human bone marrow differentiate into adipocytes instead of osteoblasts leading to a decreased number of osteoblasts and a decrease in bone mineral density (BMD). Thus, PPARs may have impacts on bone metabolism. 224 postmenopausal women (171 osteoporotic and osteopenic, 53 healthy control) were included in this study. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and agarose gel electrophoresis techniques were performed to detect PPARα L162V and PPARγ Pro12Ala/C161T polymorphisms. The distribution of PPARγ Pro12Ala genotype and allele frequencies was not statistically different in control and patient (osteopenic+osteoporotic) groups (p>0.05). However, in the patient group, subjects with “Pro12Pro” genotype had lower lumbar spine (L1-L4) BMD values than those with “Ala” allele (p 0.05). We suggested that PPARγ Pro12Ala and C161T gene variants might be contributing factors in the development of osteoporosis. Cite this article as : Kurt Şirin O, Yilmaz Aydogan H, Uyar M, Can A (2019). PPARγ Pro12Ala and C161T polymorphisms, but not PPARα L162V, are associated with osteoporosis risk in Turkish postmenopausal women. Istanbul J Pharm 49 (1): 14-19.","PeriodicalId":14484,"journal":{"name":"İstanbul Journal of Pharmacy","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"İstanbul Journal of Pharmacy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26650/ISTANBULJPHARM.2019.18005","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
DOI : 10.26650/IstanbulJPharm.2019.18005 Stimulation of peroxisome proliferator-activated receptors (PPARs) causes mesenchymal stem cells of the human bone marrow differentiate into adipocytes instead of osteoblasts leading to a decreased number of osteoblasts and a decrease in bone mineral density (BMD). Thus, PPARs may have impacts on bone metabolism. 224 postmenopausal women (171 osteoporotic and osteopenic, 53 healthy control) were included in this study. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and agarose gel electrophoresis techniques were performed to detect PPARα L162V and PPARγ Pro12Ala/C161T polymorphisms. The distribution of PPARγ Pro12Ala genotype and allele frequencies was not statistically different in control and patient (osteopenic+osteoporotic) groups (p>0.05). However, in the patient group, subjects with “Pro12Pro” genotype had lower lumbar spine (L1-L4) BMD values than those with “Ala” allele (p 0.05). We suggested that PPARγ Pro12Ala and C161T gene variants might be contributing factors in the development of osteoporosis. Cite this article as : Kurt Şirin O, Yilmaz Aydogan H, Uyar M, Can A (2019). PPARγ Pro12Ala and C161T polymorphisms, but not PPARα L162V, are associated with osteoporosis risk in Turkish postmenopausal women. Istanbul J Pharm 49 (1): 14-19.
刺激过氧化物酶体增殖物激活受体(PPARs)导致人骨髓间充质干细胞分化为脂肪细胞而不是成骨细胞,导致成骨细胞数量减少和骨矿物质密度(BMD)降低。因此,ppar可能对骨代谢有影响。224名绝经后妇女(骨质疏松症和骨质减少症171名,健康对照53名)纳入本研究。采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)和琼脂糖凝胶电泳技术检测PPARα L162V和PPARγ Pro12Ala/C161T多态性。PPARγ Pro12Ala基因型和等位基因频率在对照组和患者(骨质减少+骨质疏松)组的分布无统计学差异(p < 0.05)。然而,在患者组中,“Pro12Pro”基因型受试者的腰椎(L1-L4) BMD值低于“Ala”等位基因组(p 0.05)。我们认为PPARγ Pro12Ala和C161T基因变异可能是骨质疏松症发生的促进因素。本文引自:Kurt Şirin O, Yilmaz Aydogan H, Uyar M, Can A(2019)。PPARγ Pro12Ala和C161T多态性与土耳其绝经后妇女骨质疏松风险相关,但与PPARα L162V无关。中华医学杂志,49(1):14-19。