ABSTRACT
Background: the aim of this study was to examine the interaction of dietary food groups and genetic variants of APOA1/APOC3, relative to Metabolic Syndrome [MetS] risk in adults
Methods: in this matched nested case-control study, 414 MetS subjects and 414 controls were selected from among participants of Tehran Lipid and Glucose Study. Dietary intake was assessed with the use of a valid and reliable semi-quantitative food frequency questionnaire. Single Nucleotide Polymorphisms [SNPs], APOA1 [rs670, -75G>A and rs5069,+83C>T/APOC3 rs5128 C3238>G] were genotyped by the conventional polymerase chain reaction and restriction fragment length polymorphism
Results: the mean [SD] of age was 40.7 [13] and 41.2 [13] years in male cases and controls versus 44.0 [11] and 44.0 [12] years in female case and controls. A significant interaction between intake quartiles of the sugar group and APOA1 combined group [GA+AA/CT+TT] SNPs was found; The ORs for these genotype carriers were [1, 0.44, 0.36, 0.23; P trend<0.001] in quartiles of intake, relative to other combined genotypes [P interaction=0.02]. MetS risk appeared to be increased significantly in higher quartiles of sweet beverages and fish intakes in the GA+AA/CT+TT/CC genotypes of APOA1/APOC3 SNPs, compared to other genotypes [P interaction=0.01]. The combined effect of genotypes of APOC3/APOA1 showed further decrease in MetS risk in higher quartiles of sugar group intakes [OR: 1, 0.24, 0.26, 0.14, P trend=0.001] relative to other combinations [P interaction=0.008]
Conclusion: results obtained demonstrate that some dietary food groups [sugar, fish, and sweet beverages] modulate the effect of APOA1/APOC3 SNPs in relation to MetS risk
ABSTRACT
Diabetes Mellitus [DM] is a chronic heterogeneous disorder and oxidative stress is a key participant in the development and progression of it and its complications. Antioxidant status can affect vulnerability to oxidative damage, onset and progression of diabetes and diabetes complications. Superoxide dismutase 2 [SOD2] is one of the major antioxidant defense systems against free radicals. SOD2 is encoded by the nuclear SOD2 gene located on the human chromosome 6q25 and the Ala16Val polymorphism has been identified in exon 2 of the human SOD2 gene. Ala16Val [rs4880] is the most commonly studied SOD2 single nucleotide polymorphism [SNP] in SOD2 gene. This SNP changes the amino acid at position 16 from valine [Val] to alanine [Ala], which has been shown to cause a conformational change in the target sequence of manganese superoxide dismutase [MnSOD] and also affects MnSOD activity in mitochondria. Ala16Val SNP and changes in the activity of the SOD2 antioxidant enzyme have been associated with altered progression and risk of different diseases. Association of this SNP with diabetes and some of its complications have been studied in numerous studies. This review evaluated how rs4880, oxidative stress and antioxidant status are associated with diabetes and its complications although some aspects of this line still remain unclear