Luglio Harry Freitag, Sulistyoningrum Dian Caturini, Huriyati Emy, Lee Yi Yi, Wan Muda Wan Abdul Manan
Department of Nutrition and Health, Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia.
School of Health Sciences, Universiti Sains Malaysia, Gelugor 11800, Malaysia.
Nutrients. 2017 Jul 7;9(7):716. doi: 10.3390/nu9070716.
Obesity has been associated with leptin resistance and this might be caused by genetic factors. The aim of this study was to investigate the gene-lifestyle interaction between -866G/A UCP2 (uncoupling protein 2) gene polymorphism, dietary intake and leptin in a population based study.
This is a cross sectional study conducted in adults living at urban area of Yogyakarta, Indonesia. Data of adiposity, lifestyle, triglyceride, high density lipoprotein (HDL) cholesterol, leptin and UCP2 gene polymorphism were obtained in 380 men and female adults.
UCP2 gene polymorphism was not significantly associated with adiposity, leptin, triglyceride, HDL cholesterol, dietary intake and physical activity (all > 0.05). Leptin was lower in overweight subjects with AA + GA genotypes than those with GG genotype counterparts ( = 0.029). In subjects with AA + GA genotypes there was a negative correlation between leptin concentration ( = -0.324; < 0.0001) and total energy intake and this correlation was not seen in GG genotype ( = -0.111; = 0.188).
In summary, we showed how genetic variation in -866G/A UCP2 affected individual response to leptin production. AA + GA genotype had a better leptin sensitivity shown by its response in dietary intake and body mass index (BMI) and this explained the protective effect of A allele to obesity.
肥胖与瘦素抵抗有关，这可能由遗传因素引起。本研究的目的是在一项基于人群的研究中，调查 -866G/A 解偶联蛋白 2（UCP2）基因多态性、饮食摄入与瘦素之间的基因 - 生活方式相互作用。
这是一项对印度尼西亚日惹市区成年人进行的横断面研究。在 380 名成年男性和女性中获取了肥胖、生活方式、甘油三酯、高密度脂蛋白（HDL）胆固醇、瘦素和 UCP2 基因多态性的数据。
UCP2 基因多态性与肥胖、瘦素、甘油三酯、HDL 胆固醇、饮食摄入和身体活动均无显著相关性（均 >0.05）。AA + GA 基因型的超重受试者的瘦素水平低于 GG 基因型的受试者（P = 0.029）。在 AA + GA 基因型的受试者中，瘦素浓度与总能量摄入之间存在负相关（r = -0.324；P < 0.0001），而在 GG 基因型中未观察到这种相关性（r = -0.111；P = 0.188）。
总之，我们展示了 -866G/A UCP2 的基因变异如何影响个体对瘦素产生的反应。AA + GA 基因型在饮食摄入和体重指数（BMI）方面的反应表明其具有更好的瘦素敏感性，这解释了 A 等位基因对肥胖的保护作用。
