Interactions between C-Reactive Protein Genotypes with Markers of Nutritional Status in Relation to Inflammation

被引:13
|
作者
Nienaber-Rousseau, Cornelie [1 ]
Swanepoel, Bianca [1 ]
Dolman, Robin C. [1 ]
Pieters, Marlien [1 ]
Conradie, Karin R. [1 ]
Towers, G. Wayne [1 ]
机构
[1] North West Univ, Ctr Excellence Nutr, ZA-2520 Potchefstroom, South Africa
关键词
CRP; diet-gene interactions; inflammation therapy; nutrigenetics; systemic inflammation; CORONARY-HEART-DISEASE; SYSTEMIC INFLAMMATION; AFRICAN POPULATION; RISK; PLASMA; INTERLEUKIN-6; MIDDLE; INTERVENTION; ASSOCIATION; CHOLESTEROL;
D O I
10.3390/nu6115034
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Inflammation, as indicated by C-reactive protein concentrations (CRP), is a risk factor for chronic diseases. Both genetic and environmental factors affect susceptibility to inflammation. As dietary interventions can influence inflammatory status, we hypothesized that dietary effects could be influenced by interactions with single nucleotide polymorphisms (SNPs) in the CRP gene. We determined 12 CRP SNPs, as well as various nutrition status markers in 2010 black South Africans and analyzed their effect on CRP. Interactions were observed for several genotypes with obesity in determining CRP. Lipid intake modulated the pro-inflammatory effects of some SNPs, i.e., an increase in both saturated fatty acid and monounsaturated fatty acid intake in those homozygous for the polymorphic allele at rs2808630 was associated with a larger increase in CRP. Those harboring the minor alleles at rs3093058 and rs3093062 presented with significantly higher CRP in the presence of increased triglyceride or cholesterol intake. When harboring the minor allele of these SNPs, a high omega-6 to -3 ratio was, however, found to be anti-inflammatory. Carbohydrate intake also modulated CRP SNPs, as HbA1C and fasting glucose levels interacted with some SNPs to influence the CRP. This investigation highlights the impact that nutritional status can have on reducing the inherent genetic susceptibility to a heightened systemic inflammatory state.
引用
收藏
页码:5034 / 5050
页数:17
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