Apolipoprotein A2 -265 T>C polymorphism interacts with dietary fatty acids intake to modulate inflammation in type 2 diabetes mellitus patients.

OBJECTIVE: Several investigations have been conducted regarding the interaction between Apolipoprotein A2 (APOA2) -265 T>C polymorphism and dietary intake of saturated fatty acids (SFAs) on obesity in healthy individuals or type 2 diabetes mellitus (T2 DM) patients. The aim of the present study is to examine the effect of this interaction on inflammatory markers in T2 DM patients. METHODS: This is a comparative cross-sectional study on 180 T2 DM patients with known APOA2 genotype. Dietary intake was assessed by food-frequency questionnaire and serum levels of inflammatory markers (interleukin [IL]-18, pentraxin 3, and high-sensitivity C-reactive protein [hs-CRP]) were measured. The subjects were dichotomized into "high" and "low" categories, based on the median dietary intake of polyunsaturated fatty acids (PUFAs), monounsaturated fatty acids (MUFAs), and SFAs. The data were analyzed by analysis of covariance multivariate interaction model. RESULTS: In CC genotype, higher median intake of ω-3 PUFAs and MUFAs was associated with decreased serum levels of IL-18 and hs-CRP (P = 0.014 and 0.008, respectively). In T-allele carriers, higher median intake of SFAs was associated with increased serum hs-CRP level (P < 0.001). There was a significant relationship between APOA2 polymorphism and ω-3 PUFA intake on serum IL-18 level (P interaction = 0.03). Moreover, the relationship between this polymorphism and SFA and MUFA intake on serum hs-CRP level was statistically significant (P interaction = 0.03 and 0.024, respectively). CONCLUSIONS: In T2 DM patients, the dietary intake of antiinflammatory fatty acids, such as ω-3 PUFAs and MUFAs, could reduce the inflammatory effects associated with the CC genotype. In addition, proinflammatory fatty acids, such as SFAs, could overcome the antiinflammatory effect of the T-allele. Further studies are needed to confirm these findings.

The interaction between ApoA2 -265T>C polymorphism and dietary fatty acids intake on oxidative stress in patients with type 2 diabetes mellitus.

INTRODUCTION: Apolipoprotein A2 (APOA2) -265T>C polymorphism has been studied in relation to oxidative stress and various dietary fatty acids. Since the interaction between APOA2 polymorphism and dietary fatty acids on oxidative stress has not yet discussed, we aimed to investigate the interaction on oxidative stress in type 2 diabetes mellitus (T2DM) patients. METHODS: The subjects were 180 T2DM patients with known APOA2 genotype, either TT, TC or CC. Superoxide dismutase (SOD) activity was determined by colorimetric method. Total antioxidant capacity (TAC) and serum level of 8-isoprostane F2α were measured by spectrophotometry and ELISA, respectively. Dietary intake was collected through a food frequency questionnaire. Based on the median intake, fatty acids intake was dichotomized into high or low groups. The interaction between APOA2 polymorphism and dietary fatty acids intake was analyzed by ANCOVA multivariate interaction model. RESULTS: Higher than median intake of omega-6 polyunsaturated fatty acids (n-6 PUFA) was associated with increased serum level of 8-isoprostane F2α in subjects with TT/TC genotype (p = 0.004), and higher than median intake of omega-3 polyunsaturated fatty acids (n-3 PUFA) was associated with increased serum SOD activity in CC genotype (p < 0.001). There was a statistically significant interaction between APOA2 polymorphism and n-6 PUFA intake on 8-isoprostane F2α concentration as well as n-3 PUFA intake on serum SOD activity (p-interaction = 0.04 and 0.02, respectively). CONCLUSIONS: The current study shows the interaction between APOA2 polymorphism and dietary fatty acids intake on oxidative stress. More investigations on different populations are required to confirm the interaction.

APO A2 -265T/C Polymorphism Is Associated with Increased Inflammatory Responses in Patients with Type 2 Diabetes Mellitus.

BACKGROUND: Apolipoprotein A2 (APO A2) is the second most abundant structural apolipoprotein in high density lipoprotein. Several studies have examined the possible effect of APO A2 on atherosclerosis incidence. Due to the role of inflammation in atherosclerosis, we aimed to determine the relationship between APO A2 -265T/C polymorphism and inflammation as a risk factor in type 2 diabetes mellitus (T2DM) patients. METHODS: In total, 180 T2DM patients, with known APO A2 -265T/C polymorphism, were recruited for this comparative study and were grouped equally based on their genotypes. Dietary intakes, anthropometric parameters, lipid profile, and inflammatory markers (i.e., pentraxin 3 [PTX3], high-sensitivity C-reactive protein [hs-CRP], and interleukin 18) were measured. The data were analyzed using an independent t-test, a chi-square test, and the analysis of covariance. RESULTS: After adjusting for confounding factors, in the entire study population and in the patients with or without obesity, the patients with the CC genotype showed higher hs-CRP (P=0.001, P=0.008, and P=0.01, respectively) and lower PTX3 (P=0.01, P=0.03, and P=0.04, respectively) in comparison with the T allele carriers. In the patients with the CC genotype, no significant differences were observed in the inflammatory markers between the obese or non-obese patients. However, regarding the T allele carriers, the plasma hs-CRP level was significantly higher in the obese patients compared to the non-obese patients (P=0.01). CONCLUSION: In the T2DM patients, the CC genotype could be considered as a risk factor and the T allele as a protective agent against inflammation, which the latter effect might be impaired by obesity. Our results confirmed the anti-atherogenic effect of APO A2, though more studies are required to establish this effect.

Association between ApoA-II -265T/C polymorphism and oxidative stress in patients with type 2 diabetes mellitus.

BACKGROUND: Apolipoprotein A-II (ApoA-II) constitutes approximately 20% of the total HDL protein content. The results of various studies on the relationship between cardiovascular diseases (CVD) and the plasma ApoA-II level are contradictory. The aim of this study was to determine the relationship between ApoA-II polymorphism and oxidative stress (OS) as a risk factor for CVD. METHODS: The present comparative study was carried out on 180 obese and non-obese patients with type 2 diabetes, with equal numbers of CC, TC, and TT genotypes of ApoA-II -265T/C gene. The ApoA-II genotype was determined by the TaqMan assay method. The anthropometric measurements and serum levels of lipid profile, superoxide dismutase activity (SOD), total antioxidant capacity (TAC), and 8-isoprostaneF2α were measured. RESULTS: After adjusting for confounding factors, in the total study population and in obese and non-obese groups, the subjects with CC genotype had a lower mean serum SOD activity (p=0.002, p=0.007 and p=0.005, respectively) and higher mean 8-isoprostaneF2α concentration (p<0.001, p=0.003 and p=0.004, respectively) than the T-allele carriers. In the TT/TC group, the mean 8-isoprostanF2α concentration was significantly higher in the obese subjects than the non-obese subjects (p=0.009). In the CC group, no significant differences were found in the OS factors between obese and non-obese groups. CONCLUSION: The T allele in patients with type 2 diabetes is a protective factor against OS; obesity inhibits this protective effect. The results of this study represent the anti-atherogenic properties of ApoA-II. However, further studies are needed in this field.