Obesity-induced insulin resistance via changes in the DNA methylation profile of insulin pathway genes

Adv Clin Exp Med. 2019 Dec;28(12):1599-1607. doi: 10.17219/acem/110321.

Abstract

Background: Obesity has been shown to play a key role in the development of insulin resistance (IR). Abundant data implicate obesity in DNA hypermethylation at global and site-specific levels, including genes regulating insulin sensitivity. Deregulation of epigenetic marks implicates gene expression and changes in cell metabolism.

Objectives: Our previous reports demonstrated that the strongest risk factor in the development of IR is BMI; accordingly, the objective of this study was to investigate the effect of obesity on DNA methylation and insulin sensitivity.

Material and methods: A study was carried out on lymphocytes (N-34) and visceral adipose tissue (VAT; N-35) of insulin-resistant subjects and healthy controls. Genetic material (DNA and RNA) was extracted from cells. Global and site-specific DNA methylation was analyzed with the use of restriction enzymes followed by real-time polymerase chain reaction (PCR). Gene expression was analyzed as relative mRNA level normalized to a housekeeping gene.

Results: Global DNA methylation increased in both types of tissue in obese and insulin-resistant individuals and correlated positively with IR. Two of the 3 investigated promoters of insulin pathway genes were hypermethylated, which correlated negatively with gene expression and positively with IR. The DNMT3a gene was upregulated in obese insulin-resistant individuals in both types of tissues and correlated positively with global DNA methylation.

Conclusions: DNA methylation profile changed depending on body mass index (BMI) and influenced glucose metabolism and insulin sensitivity in VAT.

Keywords: DNA methylation; insulin resistance; insulin signaling pathway; obesity.

MeSH terms

  • Body Mass Index*
  • Case-Control Studies
  • DNA Methylation*
  • Humans
  • Insulin / metabolism*
  • Insulin Resistance*
  • Intra-Abdominal Fat
  • Obesity / metabolism*

Substances

  • Insulin