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Dis Markers. 2014;2014:758232. doi: 10.1155/2014/758232. Epub 2014 Nov 17.

Influence of adiposity-related genetic markers in a population of saudi arabians where other variables influencing obesity may be reduced.

Author information

1
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia.
2
MRC Integrative Epidemiology Unit, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK ; Bristol Genetic Epidemiology Laboratories, Department of Social and Community Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK.
3
Biomarkers Research Program, Biochemistry Department, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia ; Prince Mutaib Chair for Biomarkers of Osteoporosis, Biochemistry Department, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia.
4
Bristol Genetic Epidemiology Laboratories, Department of Social and Community Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK.
5
Department of Pathology and Laboratory Medicine (1122), King Fahad National Guard Hospital, King Saud Bin Abdulaziz University for Health Sciences, P.O. Box 22490, Riyadh 11426, Saudi Arabia.

Abstract

Large scale studies in Europeans have clearly identified common polymorphism affecting BMI and obesity. We undertook a genotype study to examine the impact of variants, known to influence obesity, in a sample from the Saudi Arabian population, notable for its profound combination of low mean physical activity indices and high energy intake. Anthropometry measures and genotypes were obtained for 367 Saudis, taken from King Saud University and Biomarker Screening Project in Riyadh (Riyadh Cohort). We observed large effect sizes with obesity for rs10767664 (BDNF) (OR = 1.923, P = 0.00072) and rs3751812 (FTO) (OR = 1.523, P = 0.016) in our sample and, using weighted genetic risk scores, we found strong evidence of a cumulative effect using 11 SNPs taken predominantly from loci principally affecting appetite (OR = 2.57, P = 0.00092). We used conditional analyses to discern which of our three highly correlated FTO SNPs were responsible for the observed signal, although we were unable to determine with confidence which best marked the causal site. Our analysis indicates that markers located in loci known to influence fat mass through increased appetite affect obesity in Saudi Arabians to an extent possibly greater than in Europeans. Larger scale studies will be necessary to obtain a precise comparison.

PMID:
25484485
PMCID:
PMC4251424
DOI:
10.1155/2014/758232
[Indexed for MEDLINE]
Free PMC Article

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