APO A2 -265T/C Polymorphism Is Associated with Increased Inflammatory Responses in Patients with Type 2 Diabetes Mellitus.
10.4093/dmj.2016.40.3.222
- Author:
Fariba KOOHDANI
1
;
Haleh SADRZADEH-YEGANEH
;
Mahmoud DJALALI
;
Mohammadreza ESHRAGHIAN
;
Elham ZAMANI
;
Gity SOTOUDEH
;
Mohammad Ali MANSOURNIA
;
Laleh KERAMAT
Author Information
1. Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran. laleh_keramat@yahoo.com
- Publication Type:Comparative Study ; Original Article
- Keywords:
Apolipoprotein A-II;
Diabetes;
Inflammatory response;
Obesity;
Polymorphism
- MeSH:
Alleles;
Apolipoprotein A-II*;
Apolipoproteins;
Atherosclerosis;
C-Reactive Protein;
Diabetes Mellitus, Type 2*;
Genotype;
Humans;
Incidence;
Inflammation;
Interleukins;
Lipoproteins;
Obesity;
Plasma;
Risk Factors
- From:Diabetes & Metabolism Journal
2016;40(3):222-229
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
