Abstract

The objective of this study was to explore the effects of dietary acid load (DAL) and IGF1 and IL6 gene polymorphisms and their potential diet–gene interactions on metabolic traits. A total of 211 community-dwelling postmenopausal women were recruited. DAL was estimated using potential renal acid load (PRAL). Blood was drawn for biochemical parameters and DNA was extracted and Agena® MassARRAY was used for genotyping analysis to identify the signalling of IGF1 (rs35767 and rs7136446) and IL6 (rs1800796) polymorphisms. Interactions between diet and genetic polymorphisms were assessed using regression analysis. The result showed that DAL was positively associated with fasting blood glucose (FBG) (β = 0.147, p < 0.05) and there was significant interaction effect between DAL and IL6 with systolic blood pressure (SBP) (β = 0.19, p = 0.041). In conclusion, these findings did not support the interaction effects between DAL and IGF1 and IL6 single nucleotide polymorphisms (rs35767, rs7136446, and rs1800796) on metabolic traits, except for SBP. Besides, higher DAL was associated with higher FBG, allowing us to postulate that high DAL is a potential risk factor for diabetes.

Highlights

  • Metabolic syndrome (MS) is a cluster of interrelated and heritable metabolic traits, which collectively impart unsurpassed risk for type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease [1]

  • Genome-wide studies have identified that insulin growth factors 1 (IGF1) and interleukin 6 (IL6) gene polymorphisms are responsible for metabolic traits

  • Previous studies showed that IL6 gene-587 G/A polymorphism increased the risk of T2DM in G-allele carriers close to

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Summary

Introduction

Metabolic syndrome (MS) is a cluster of interrelated and heritable metabolic traits, which collectively impart unsurpassed risk for type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease [1]. The etiology of MS is likely multifactorial and involves the interplay among lifestyle behavior, ageing, obesogenic environments, and genetic susceptibility [4], with the latter having ignited the interest for numerous genetic studies in Asia to gain insight into the genetic basis of MS and its component traits [5,6,7,8,9,10,11]. Lifestyle is a well-known determinant for the development of MS, genetic variants, especially when they involve functional polymorphisms in the promoter regions of the genes, may alter the function and the expression of genes that are associated with energy intake and energy expenditure [12]. Genome-wide studies have identified that insulin growth factors 1 (IGF1) and interleukin 6 (IL6) gene polymorphisms are responsible for metabolic traits. Previous studies showed that IL6 gene-587 G/A polymorphism increased the risk of T2DM in G-allele carriers close to

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