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      Association between the APOA2 promoter polymorphism and body-weight in Mediterranean and Asian populations. Replication of a gene-saturated fat interaction

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          Abstract

          Objective

          The APOA2 gene has been associated with obesity and insulin resistance (IR) in animal and human studies with controversial results. We have reported an APOA2-saturated fat interaction determining body mass index (BMI) and obesity in American populations. This work aims to extend our findings to European and Asian populations.

          Methods

          Cross-sectional study in 4602 subjects from 2 independent populations: A high cardiovascular risk Mediterranean population (n=907 men and women; aged 67+/−6 years) and a multiethnic Asian population (n=2506 Chinese, n=605 Malays and n=494 Asian Indians; aged 39+/−12 years), participating in a Singapore National Health Survey. Anthropometric, clinical, biochemical, lifestyle and dietary variables were determined. Homeostasis model assessment of IR (HOMA-IR) was used in Asians. We analyzed gene-diet interactions between the APOA2 −265T>C polymorphism and saturated fat intake (<or>=22 g/d) on anthropometric measures and IR.

          Results

          Frequency of CC subjects differed among populations (1%–15%). We confirmed a recessive effect of the APOA2 polymorphism, and replicated the APOA2–saturated fat interaction on body-weight. In Mediterranean individuals, the CC genotype was associated with a 6.8% greater BMI in those consuming a high (P=0.018), but not a low (P=0.316) saturated fat diet. Likewise, the CC genotype was significantly associated with higher obesity prevalence in Chinese and Asian Indians only with a high-saturated fat intake (P=0.036). We also found a significant APOA2-saturated fat interaction in determining IR in Chinese and Asian Indians (P=0.026).

          Conclusion

          The influence of the APOA2 −265T>C polymorphism on body-weight-related measures was modulated by saturated fat in Mediterranean and Asian populations.

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          Most cited references35

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          Six new loci associated with body mass index highlight a neuronal influence on body weight regulation.

          Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
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            Asians are different from Caucasians and from each other in their body mass index/body fat per cent relationship.

            The objective was to study the relationship between body mass index (BMI) and body fat per cent (BF%) in different population groups of Asians. The study design was a literature overview with special attention to recent Asian data. Specific information is provided on Indonesians (Malays and Chinese ancestry), Singaporean Chinese, Malays and Indians, and Hong Kong Chinese. The BMI was calculated from weight and height and the BF% was determined by deuterium oxide dilution, a chemical-for-compartment model, or dual-energy X-ray absorptiometry. All Asian populations studied had a higher BF% at a lower BMI compared to Caucasians. Generally, for the same BMI their BF% was 3-5% points higher compared to Caucasians. For the same BF% their BMI was 3-4 units lower compared to Caucasians. The high BF% at low BMI can be partly explained by differences in body build, i.e. differences in trunk-to-leg-length ratio and differences in slenderness. Differences in muscularity may also contribute to the different BF%/BMI relationship. Hence, the relationship between BF% and BMI is ethnic-specific. For comparisons of obesity prevalence between ethnic groups, universal BMI cut-off points are not appropriate.
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              The human obesity gene map: the 2005 update.

              This paper presents the 12th update of the human obesity gene map, which incorporates published results up to the end of October 2005. Evidence from single-gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, transgenic and knockout murine models relevant to obesity, quantitative trait loci (QTL) from animal cross-breeding experiments, association studies with candidate genes, and linkages from genome scans is reviewed. As of October 2005, 176 human obesity cases due to single-gene mutations in 11 different genes have been reported, 50 loci related to Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and causal genes or strong candidates have been identified for most of these syndromes. There are 244 genes that, when mutated or expressed as transgenes in the mouse, result in phenotypes that affect body weight and adiposity. The number of QTLs reported from animal models currently reaches 408. The number of human obesity QTLs derived from genome scans continues to grow, and we now have 253 QTLs for obesity-related phenotypes from 61 genome-wide scans. A total of 52 genomic regions harbor QTLs supported by two or more studies. The number of studies reporting associations between DNA sequence variation in specific genes and obesity phenotypes has also increased considerably, with 426 findings of positive associations with 127 candidate genes. A promising observation is that 22 genes are each supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. The electronic version of the map with links to useful publications and relevant sites can be found at http://obesitygene.pbrc.edu.
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                Author and article information

                Journal
                101256108
                32579
                Int J Obes (Lond)
                International journal of obesity (2005)
                0307-0565
                1476-5497
                18 August 2010
                26 October 2010
                May 2011
                1 November 2011
                : 35
                : 5
                : 666-675
                Affiliations
                [1 ]Nutrition and Genomics Laboratory, JM-USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA
                [2 ]Genetic and Molecular Epidemiology Unit School of Medicine. University of Valencia, Valencia, Spain
                [3 ]CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
                [4 ]Department of Endocrinology, Singapore General Hospital, Singapore
                [5 ]Epidemiology and Disease Control Division, Ministry of Health Singapore, Singapore
                [6 ]Department of Computing Languages and Systems. Universitat Jaume I. Castellon, Spain.
                [7 ]Reina Sofia University Hospital, Lipids and Atherosclerosis Research Unit, University of Cordoba, Cordoba, Spain
                [8 ]Department of Internal Medicine. Hospital Clinic, Barcelona, Spain
                [9 ]Department of Cardiovascular Epidemiology and Population Genetics, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain
                Author notes
                [* ] Correspondence to: Jose M. Ordovas. Director, Nutrition and Genomics Laboratory, JM-USDA Human Nutrition, Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111-1524, USA. Tel: (617) 556-3102. Fax: (617) 556-3211, jose.ordovas@ 123456tufts.edu
                Article
                nihpa225024
                10.1038/ijo.2010.187
                3030929
                20975728
                a1108f31-e215-47b8-9fc3-1d7138bfa034

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                History
                Funding
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 HL054776-13 ||HL
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 DK075030-03 ||DK
                Categories
                Article

                Nutrition & Dietetics
                insulin resistance,gene-diet interaction,obesity,saturated fat,apoa2
                Nutrition & Dietetics
                insulin resistance, gene-diet interaction, obesity, saturated fat, apoa2

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