The relationship between dietary fatty acids and inflammatory genes on the obese phenotype and serum lipids - PubMed (original) (raw)

Review

The relationship between dietary fatty acids and inflammatory genes on the obese phenotype and serum lipids

Yael T Joffe et al. Nutrients. 2013.

Abstract

Obesity, a chronic low-grade inflammatory condition is associated with the development of many comorbidities including dyslipidemia. This review examines interactions between single nucleotide polymorphisms (SNP) in the inflammatory genes tumor necrosis alpha (TNFA) and interleukin-6 (IL-6) and dietary fatty acids, and their relationship with obesity and serum lipid levels. In summary, dietary fatty acids, in particular saturated fatty acids and the omega-3 and omega-6 polyunsaturated fatty acids, impact the expression of the cytokine genes TNFA and IL-6, and alter TNFα and IL-6 production. In addition, sequence variants in these genes have also been shown to alter their gene expression and plasma levels, and are associated with obesity, measures of adiposity and serum lipid concentrations. When interactions between dietary fatty acids and TNFA and IL-6 SNPs on obesity and serum lipid were analyzed, both the quantity and quality of dietary fatty acids modulated the relationship between TNFA and IL-6 SNPs on obesity and serum lipid profiles, thereby impacting the association between phenotype and genotype. Researching these diet-gene interactions more extensively, and understanding the role of ethnicity as a confounder in these relationships, may contribute to a better understanding of the inter-individual variability in the obese phenotype.

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Figures

Figure 1

A proposed schematic diagram for obesity-associated low-grade inflammation, and the relationship of diet–gene interactions on obesity and dyslipidemia. Adipocytes become hypertrophic through over-nutrition. Expansion of adipose tissue in obesity leads to a subsequent increase in the production of chemokines by the adipocytes, resulting in increasing macrophage infiltration and enhanced production of pro-inflammatory cytokines, such as TNFα and IL-6. Obesity-associated low-grade inflammation results in an increase in serum trigycerides, and LDL-C concentrations and is associated with dyslipidemia. Environmental factors and DNA sequence variations in inflammatory genes, interact to impact molecular processes of the inflammatory pathway, serum lipids and the obese phenotype. APOA, Apolipoprotein A; APOB, Apolipoprotein B; APOE, Apolipoprotein E; CRP, C-reactive protein; IL-6, interleukin-6; LDL-C, low-density lipoprotein cholesterol; MCP-1, monocyte chemotactic protein-1; PAI, plasminogen activated inhibitor; PPARγ, peroxisome proliferator-activated receptor gamma; TAG, triglycerides; TNFα, tumor necrosis factor.

Figure 2

The modeled relationship between the odds of being obese (odds of being obese vs. being normal weight), _TNFA_–308 genotype and dietary fat intake (%E) for black SA women. The curve gives the modeled obesity OR for genotype GA+AA versus genotype GG, at each fat intake (%E). Lines show the total dietary fat intake (%E) of equal odds (OR = 1, for the genotype groups), namely 40.6 (%E), the OR for fat intake = 30 (%E) namely 0.12 and the OR for fat intake = 35 (%E), namely 0.33 [3].

Figure 3

The relationship between BMI and fat mass, IL-6 –174 G>C, IVS3+281 G>T and IVS4+869 A>G polymorphisms and dietary fat intake in white SA women. Symbols represent observed values for each woman. The lines are modeled relationships for a woman of average age (27.3 years) [98]. (A) With increasing _n_-3 PUFA intake (%E), BMI decreased in those with the –174 CC or GC genotypes. (B) With increasing _n_-6:_n_-3 PUFA ratio, BMI increased equally with each additional –174 C allele. (C) With increasing ALA intake (%E), BMI decreased with each additional IVS3+281 T allele. (D) With increasing _n_-6:_n_-3 PUFA ratio, BMI increased with each additional IVS3+281T allele. (E) With increasing ALA intake (%E), fat mass decreased in those with the IVS4+869 AG or GG genotype. (F) With increasing _n_-6:_n_-3 PUFA ratio, fat mass increased in those with the IVS4+869 AG or GG genotype; compared to those with the AA genotype.

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The relationship between dietary fatty acids and inflammatory genes on the obese phenotype and serum lipids - PubMed (original) (raw)