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The interaction between a functional apolipoprotein A2 gene (APOA2) variant and saturated fatty acids (SFAs) for the outcome of body mass index (BMI) is among the most widely replicated gene-nutrient interactions. Whether this interaction can be extrapolated to food-based sources of SFAs, specifically dairy foods, is unexplored. Cross-sectional analyses were performed in 2 U.S. population--based samples. We evaluated interactions between dairy foods and APOA2 2265T > C (rs5082) for BMI in the Boston Puerto Rican Health Study (n = 955) and tested for replication in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study (n = 1116). Dairy products were evaluated as total dairy, higher-fat dairy (>1%), and low-fat dairy (≤1%) in servings per day, dichotomized into high and low based on each population median and also as continuous variables. We identified a statistically significant interaction between the APOA2 2265T > C variant and higher-fat dairy food intake in the Boston Puerto Ricans (P-interaction = 0.028) and replicated this relation in the GOLDN study (P-interaction = 0.001). In both groups, individuals with the previously demonstrated SFA-sensitive genotype (CC) who consumed a greater amount of higher-fat dairy foods had greater BMI (P = 0.013 in Boston Puerto Ricans; P = 0.0007 in GOLDN women) compared with those consuming less of the higher-fat dairy foods. The results expand the understanding of the metabolic influence of dairy products, an important food group for which variable relations to body weight may be in part genetically based. Moreover, these findings suggest that other strongly demonstrated gene-nutrient relations might be investigated through appropriate food-based, translatable avenues and may be relevant to dietary management of obesity. [ABSTRACT FROM AUTHOR]

Evidence that physical activity (PA) modulates the association between the fat mass and obesity-associated gene (FTO) and BMI is emerging; however, information about dietary factors modulating this association is scarce. We investigated whether fat and carbohydrate intake modified the association of FTO gene variation with BMI in two populations, including participants in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study (n = 1069) and in the Boston Puerto Rican Health (BPRHS) study (n = 1094). We assessed energy, nutrient intake, and PA using validated questionnaires. Genetic variability at the FTO locus was characterized by polymorphisms rs9939609 (in the GOLDN) and rs1121980 (in the GOLDN and BPRHS). We found significant interactions between PA and FTO on BMI in the GOLDN but not in the BPRHS. We found a significant interaction between SFA intake and FTO on BMI, which was stronger than that of total fat and was present in both populations (P-interaction = 0.007 in the GOLDN and P-interaction = 0.014 in BPRHS for categorical; and P-interaction = 0.028 in the GOLDN and P-interaction = 0.041 in BPRHS for continuous SFA). Thus, homozygous participants for the FTO-risk allele had a higher mean BMI than the other genotypes only when they had a high-SFA intake (above the population mean: 29.7 ± 0.7 vs. 28.1 ± 0.5 kg/m²; P = 0.037 in the GOLDN and 33.6. ± 0.8 vs. 31.2 ± 0.4 kg/m²; P = 0.006 in BPRHS). No associations with BMI were found at lower SFA intakes. We found no significant interactions with carbohydrate intake. In conclusion, SFA intake modulates the association between FTO and BMI in American populations. [ABSTRACT FROM AUTHOR]

The article presents a study on the interaction among functional APOA2 polymorphism, food intake and body mass index (BMI) through the replication of a gene-diet interaction in three independent populations. It outlines the importance of characterizing gene-environment interactions since they are essential for the translation of genomics into clinical medicine. It notes that the gene-diet interaction which influence BMI and obesity have been strongly and consistently replicated.