DNA methylation of the Klf14 gene region in whole blood cells provides prediction for the chronic inflammation in the adipose tissue

Biochem Biophys Res Commun. 2018 Mar 11;497(3):908-915. doi: 10.1016/j.bbrc.2017.12.104. Epub 2018 Feb 6.

Abstract

Krüppel-Like Factor 14 (KLF14) gene, which appears to be a master regulator of gene expression in the adipose tissue and have previously been associated with BMI and Type 2 diabetes (T2D) by large genome-wide association studies. In order to find predictive biomarkers for the development of T2D, it is necessary to take epigenomic changes affected by environmental factors into account. This study focuses on ageing and obesity, which are T2D risk factors, and examines epigenetic changes and inflammatory changes. We investigated DNA methylation changes in the Klf14 promoter region in different organs of mice for comparing aging and weight. We found that methylation levels of these sites were increased with aging and weight in the spleen, the adipose tissue, the kidney, the lung, the colon and the whole blood cells. In addition, in the spleen, the adipose tissue and the whole blood, these epigenetic changes were also significantly associated with inflammatory levels. Moreover, not only Klf14, but also expression levels of some downstream genes were decreased with methylation in the spleen, the adipose tissue and the whole blood cells. Taken together, our results suggest that methylation changes of Klf14 in those tissues may be associated with changes in gene expression and inflammation on the adipose tissue of obesity and T2D. In addition, the methylation changes in the whole blood cells may serve as a predictive epigenetic biomarker for the development of T2D.

Keywords: Ageing; DNA methylation; Inflammation; Klf14; Obesity; T2D.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism
  • Adipose Tissue / pathology*
  • Aging
  • Animals
  • Chronic Disease
  • DNA Methylation*
  • Epigenesis, Genetic
  • Female
  • Inflammation / genetics*
  • Inflammation / pathology
  • Kruppel-Like Transcription Factors / genetics*
  • Male
  • Mice, Inbred C57BL
  • Obesity / genetics*
  • Obesity / pathology

Substances

  • Klf14 protein, mouse
  • Kruppel-Like Transcription Factors