Department of Medical Genetics, Faculty of Medicine, Near East University, Nicosia, Cyprus.
Department of Biochemistry, Faculty of Pharmacy, Near East University, Near East Boulevard, ZIP. 99138, Nicosia, Cyprus.
Mol Biol Rep. 2019 Oct;46(5):5425-5432. doi: 10.1007/s11033-019-04997-z. Epub 2019 Jul 30.
Obesity is a complex disorder that is influenced by genetic and environmental factors. DNA methylation is an epigenetic mechanism that is involved in development of obesity and its metabolic complications. The aim of this study was to investigate the association between the RANKL and c-Fos gene methylation on obesity with body mass index (BMI), lipid parameters, homeostasis model assessment of insulin resistance (HOMA-IR), plasma leptin, adiponectin and resistin levels. The study included 68 obese and 46 non-obese subjects. Anthropometric parameters, including body weight, body mass index, waist circumference, and waist-hip ratio, were assessed. Serum glucose, triglycerides (TG), total cholesterol, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C), plasma leptin, adiponectin and resistin levels were measured. Methylation status of RANKL and c-Fos gen were evaluated by MS-HRM. Statistically significant differences were observed between obese patients and the controls with respect to RANKL and c-Fos gene methylation status (p < 0.001). Also, statistically significant importance was observed RANKL gene methylation and increased level of leptin in obese subjects (p = 0.0081). At the same time, statistically significant association between methylation of c-Fos and increased level of adiponectin was observed in obese patients (p = 0.03) On the other hand, decreased level of resistin was observed where the c-Fos was unmetyladed in controls (p = 0.01). We conclude that methylation of RANKL and c-Fos genes have significant influences on obesity and adipokine levels. Based on literature this was the first study which shows the interactions between RANKL and c-Fos methylation and obesity.
肥胖是一种复杂的疾病,受遗传和环境因素的影响。DNA 甲基化是一种表观遗传机制,参与肥胖及其代谢并发症的发生。本研究旨在探讨 RANKL 和 c-Fos 基因甲基化与肥胖的关系,及其与体重指数(BMI)、血脂参数、胰岛素抵抗的稳态模型评估(HOMA-IR)、血浆瘦素、脂联素和抵抗素水平的关系。本研究纳入了 68 名肥胖患者和 46 名非肥胖者。评估了包括体重、体重指数、腰围和腰臀比在内的人体测量参数。测量了血清葡萄糖、甘油三酯(TG)、总胆固醇、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C)、血浆瘦素、脂联素和抵抗素水平。通过 MS-HRM 评估了 RANKL 和 c-Fos 基因的甲基化状态。肥胖患者与对照组在 RANKL 和 c-Fos 基因甲基化状态方面存在统计学显著差异(p<0.001)。此外,在肥胖患者中还观察到 RANKL 基因甲基化与瘦素水平升高之间存在统计学显著相关性(p=0.0081)。同时,在肥胖患者中观察到 c-Fos 甲基化与脂联素水平升高之间存在统计学显著相关性(p=0.03)。另一方面,在对照组中,c-Fos 未甲基化时,抵抗素水平降低(p=0.01)。我们得出结论,RANKL 和 c-Fos 基因的甲基化对肥胖和脂肪因子水平有显著影响。根据文献,这是首次表明 RANKL 和 c-Fos 甲基化与肥胖之间相互作用的研究。