Summary: Changes in postprandial small TRL TG differed among groups over time (Pgeno 3 time=0.034) whereby TT and CT subjects maintained lower concentrations throughout most of the postprandial period compared with CC subjects. Significant differences occurred at h 1, 2, 4, and 5 (P , 0.05). Postprandial changes in large TRL TG (Pgeno 3 time = 0.923) or total TG (Pgeno 3 time=0.529) did not differ by genotype.

Summary: High concentrations of adipose tissue ALA were associated with lower Prevalence Ratios of the metabolic syndrome compared with low ALA (0.81; 95% CI: 0.66, 1.00, for the comparison between the highest and the lowest quintiles; P for trend , 0.02). Higher concentrations of adipose tissue ALA were associated with a lower PR among homozygote (0.67; 95% CI: 0.53, 0.86) and heterozygote (0.84; 95% CI: 0.72, 0.99) carriers of the FADS2 T allele, but not among homozygote carriers of the deletion variant allele (0.99; 95% CI: 0.78, 1.27; P for interaction: 0.08).

Summary: No statistical heterogeneity of the effects by sex (P =0.2) was found; thus, men and women were analyzed together. Significant interactions were observed between the genotype at the PPARA locus and dietary Polyunsaturated Fats intake in the determination of serum TG (P=0.048) and apoC-III (P=0.01) concentrations. In both instances, those with the 162V allele had lower concentrations of TG and apoC-III with higher intake of Polyunsaturated Fats. In contrast, among homozygotes for the 162L allele, Polyunsaturated Fats intake did not decrease either TG or apoC-III concentrations.

Summary: PPARA is involved in the homeostasis of lipids in the fasting state as well as during the acute postprandial response to dietary fat. The minor allele carriers displayed lower mean concentrations of TG and cholesterol throughout the postprandial period. These data suggest that PPARA variants may modulate the risk of Cardiovascular disease by influencing both fasting and postprandial lipid.

Summary: After the high-P:S diet, a significant gene-by-diet interaction was observed for changes in plasma total cholesterol, apolipoprotein (apo) A-I, and cholesterol concentrations in small LDL particles (P

Summary: At baseline, PPARA Leu162Val * PPARG Pro12Ala genotype interaction did not significantly influence plasma lipid concentrations. After dietary intervention, gene-gene interaction significantly influenced LDL cholesterol (p = 0.0002) and small dense LDL as a proportion of LDL (p = 0.005) after adjustments.

Summary: Following n-3 Polyunsaturated Fats supplementation, plasma TAG concentrations of minor allele carriers of rs1799983 were considerably more responsive to changes in plasma n-3 polyunsaturated Fats, than major allele homozygotes.

Summary: A significant gene-diet interaction effect for plasma CRP concentrations was also observed. Carriers and noncarriers of the PPAR L162V polymorphism showed opposite changes, carriers of the V162 allele exhibited increased CRP values with the n–3 Polyunsaturated Fats supplementation while homozygotes of the L162 allele showed a decreased CRP value with n–3 Polyunsaturated Fats supplementation.

Summary: The 2-h postload glucose and serum insulin concentrations were higher in -308A allele carriers than in -08G/G individuals homozygous for the TNF-_x005F_x0002_gene. Individuals with Type 2 Diabetes Mellitus and the -308A allele had higher sTNFR2 and lower adiponectin concentrations than -308G homozygotes.