Published online May 15, 2015. doi: 10.4239/wjd.v6.i4.642
Peer-review started: November 1, 2014
First decision: December 26, 2014
Revised: January 29, 2015
Accepted: February 9, 2015
Article in press: February 12, 2015
Published online: May 15, 2015
Inflammation plays a significant role in the etiology of type 2 diabetes mellitus (T2DM). The rise in the pro-inflammatory cytokines is the essential step in glucotoxicity and lipotoxicity induced mitochondrial injury, oxidative stress and beta cell apoptosis in T2DM. Among the recognized markers are interleukin (IL)-6, IL-1, IL-10, IL-18, tissue necrosis factor-alpha (TNF-α), C-reactive protein, resistin, adiponectin, tissue plasminogen activator, fibrinogen and heptoglobins. Diabetes mellitus has firm genetic and very strong environmental influence; exhibiting a polygenic mode of inheritance. Many single nucleotide polymorphisms (SNPs) in various genes including those of pro and anti-inflammatory cytokines have been reported as a risk for T2DM. Not all the SNPs have been confirmed by unifying results in different studies and wide variations have been reported in various ethnic groups. The inter-ethnic variations can be explained by the fact that gene expression may be regulated by gene-gene, gene-environment and gene-nutrient interactions. This review highlights the impact of these interactions on determining the role of single nucleotide polymorphism of IL-6, TNF-α, resistin and adiponectin in pathogenesis of T2DM.
Core tip: Single nucleotide polymorphisms (SNPs) in inflammatory cytokines play role in insulin resistance and type 2 diabetes mellitus (T2DM). These SNPs are found to be correlated with cytokine serum levels, body mass index, insulin resistance and dyslipidemia although these findings are challenged by other studies. Gene-gene, gene-environment and gene-nutrient interactions alter the impact of these SNPs in pathogenesis of T2DM. These interactions may explain the inter-ethnic variations in role of inflammatory cytokines in T2DM reported in international studies. This mini-review highlights these gene-genes, gene-environment and gene-nutrient interactions and their impact on inflammatory cytokine SNPs.