Dietary patterns interact with APOA1/APOC3 polymorphisms to alter the risk of the metabolic syndrome: the Tehran Lipid and Glucose Study

Abstract

The interaction of genetic and dietary factors, as an area of CVD research, has been explored poorly. The aim of the present study was to examine the interaction of dietary patterns and three genetic variants of APOA1 and APOC3, both independently and in combination, relative to the risk of the metabolic syndrome (MetS) in Tehranian adults. In the present matched, nested case -control study, 414 subjects with the MetS and 414 controls were selected from the participants of the Tehran Lipid and Glucose Study. Dietary patterns were determined by factor analysis. APOC3 (rs5128 3238C . G) and APOA1 (rs670, 275G. A and rs5069,þ83C.T) SNP were genotyped by the conventional PCR followed by the restriction fragment length polymorphism technique. Overall, three major dietary patterns were extracted: healthy dietary pattern (HDP); Western dietary pattern (WDP); fat -sweet dietary pattern (FSDP). The A and T allele carriers of the APOA1 SNP had a greater risk of developing the MetS in the highest quartile of WDP scores (OR 3·22, 95 % CI 1·21, 8·58, P interaction ¼ 0·03). Compared with other genotype combinations, the combined effect of APOC3/APOA1 (CC/GA þ AA/CT þ TT) genotypes showed a further increase in the risk of the MetS in the highest quartile of WDP scores (OR 1, 2·49, 8·73, 6·32, P trend , 0·001, P interaction ¼ 0·003). A significant interaction was found between the quartiles of FSDP scores and the APOA1 diplotype (GA þ AA/CT þ TT). OR for these genotype carriers were 1, 0·65, 0·57 and 0·22 (P trend ¼ 0·006) in the lowest to the highest quartile of FSDP scores when compared with the other combined genotypes (P interaction ¼ 0·03). Our findings suggest that the WDP and FSDP are associated with APOA1 and APOC3 SNP in relation to the risk of the MetS.

A common variant association study in ethnic Saudi Arabs reveals novel susceptibility loci for hypertriglyceridemia

“…The encoded APOA1 protein is a cofactor for the lecithin cholesterol acyltransferase, which plays an important role in the cholesterol reverse transport by promoting its efflux from tissue to the liver for excretion. Not surprisingly, by virtue of the APOA1 protein function in cholesterol efflux, mutations in the encoding gene have recently been implicated in disorders of the lipoprotein metabolism, such as high-density lipoprotein deficiency type 1 (HDLD1) and type 2 (HDLD2) as well as metabolic syndrome (28)(29)(30). Hence, the strong link of this variant to hTG observed in this study unequivocally points to a central role for the APOA1 gene in this disorder.…”

“…Not surprisingly, by virtue of the APOA1 protein function in cholesterol efflux, mutations in the encoding gene have recently been implicated in disorders of the lipoprotein metabolism, such as high-density lipoprotein deficiency type 1 (HDLD1) and type 2 (HDLD2) as well as metabolic syndrome (28)(29)(30). Thereby, the rs1558861 on the APOA1 conspicuously exhibited disease-causative characteristics.…”

Guide for Current Nutrigenetic, Nutrigenomic, and Nutriepigenetic Approaches for Precision Nutrition Involving the Prevention and Management of Chronic Diseases Associated with Obesity

“…Interestingly, SNPs in the vitamin D receptor ( VDR ) gene, which affect vitamin D availability [20,21], have been associated with osteoporosis predisposition in postmenopausal women with low calcium intakes [22]. Moreover, SNPs in genes encoding lipid proteins such as apolipoprotein C3 ( APOC3 ) and apolipoprotein A1 ( APOA1 ) conferred a higher risk of metabolic syndrome in subjects with a Western dietary pattern [23,24]. Likewise, a genetic variant in the cytochrome P450 family 1 subfamily A member 2 ( CYP1A2 ) gene was associated with an increased risk of hypertension and CVD in moderate and heavy coffee drinkers [25,26].…”

Influence of multiple apolipoprotein A-I and B genetic variations on insulin resistance and metabolic syndrome in obstructive sleep apnea

“…The APOA-I gene is believed to be stimulated by insulin through SP-1 binding elements [48], and genetic variations of APOA-I may affect the binding site. Genediet interactions may also contribute to MetS [49,50]. Because APOB SNPs are related to lipids [51,52], the GRS of APOB may be beyond the interval of the association with insulin resistance.…”