Lack of evidence for intermolecular epistatic interactions between adiponectin and resistin gene polymorphisms in Malaysian male subjects

Abstract

Epistasis (gene-gene interaction) is a ubiquitous component of the genetic architecture of complex traits such as susceptibility to common human diseases. Given the strong negative correlation between circulating adiponectin and resistin levels, the potential intermolecular epistatic interactions between ADIPOQ (SNP+45T > G, SNP+276G > T, SNP+639T > C and SNP+1212A > G) and RETN (SNP-420C > G and SNP+299G > A) gene polymorphisms in the genetic risk underlying type 2 diabetes (T2DM) and metabolic syndrome (MS) were assessed. The potential mutual influence of the ADIPOQ and RETN genes on their adipokine levels was also examined. The rare homozygous genotype (risk alleles) of SNP-420C > G at the RETN locus tended to be co-inherited together with the common homozygous genotypes (protective alleles) of SNP+639T > C and SNP+1212A > G at the ADIPOQ locus. Despite the close structural relationship between the ADIPOQ and RETN genes, there was no evidence of an intermolecular epistatic interaction between these genes. There was also no reciprocal effect of the ADIPOQ and RETN genes on their adipokine levels, i.e., ADIPOQ did not affect resistin levels nor did RETN affect adiponectin levels. The possible influence of the ADIPOQ gene on RETN expression warrants further investigation.

RETN Gene Single Nucleotide Polymorphism Profile on Triglyceride-Glucose Index as Insulin Resistance Proxy Among Cohort Population of Non-Communicable Diseases in Bogor

“…From the results of multivariate analysis, there are indications that the RETN gene polymorphism does not work alone and may involve interactions with other factors or even genes in causing insulin resistance. 3,31,32 The RETN gene is a gene whose function is to regulate glucose homeostasis and adipogenesis. In humans, the resistin protein expressed by this gene competes with lipopolysaccharides when it binds to toll-like receptor 4 (TLR4) mononuclear cells so that it is thought to mediate cellular inflammatory processes in various diseases, including diabetes mellitus.…”

The use of weighted multiple linear regression to estimate QTL-by-QTL epistatic effects

“…The inheritance of quantitative traits has been described as a “moving target” since these traits are affected not only by the actions of multiple individual genes but also by the interaction between genes ( Lukens and Doebley, 1999 ). In this context, information on additive-by-additive interaction epistatic effects can be useful in traditional breeding programs ( Sharmila et al , 2007 ; Bnejdi and El Gazzah, 2010 ; Bnejdi et al , 2010 ; da Silva Guimarães et al , 2010 ; Lau and Muniandy, 2012 ).…”