Affiliations 

  • 1 Department of Nutrition and Health, Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia. harryfreitag@ugm.ac.id
  • 2 Department of Nutrition and Health, Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia. dian.csulis@gmail.com
  • 3 Department of Nutrition and Health, Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia. emy_huriyati@ugm.ac.id
  • 4 School of Health Sciences, Universiti Sains Malaysia, Gelugor 11800, Malaysia. leeyy.yiyi@gmail.com
  • 5 Center for Southeast Asian Studies, Kyoto University, Kyoto 606-8501, Japan. wanmanan@gmail.com
Nutrients, 2017 Jul 07;9(7).
PMID: 28686191 DOI: 10.3390/nu9070716

Abstract

BACKGROUND: 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.

METHODS: 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.

RESULTS: UCP2 gene polymorphism was not significantly associated with adiposity, leptin, triglyceride, HDL cholesterol, dietary intake and physical activity (allp> 0.05). Leptin was lower in overweight subjects with AA + GA genotypes than those with GG genotype counterparts (p= 0.029). In subjects with AA + GA genotypes there was a negative correlation between leptin concentration (r= -0.324;p< 0.0001) and total energy intake and this correlation was not seen in GG genotype (r= -0.111;p= 0.188).

CONCLUSIONS: 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.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.