Global Transcriptome Analysis of Brown Adipose Tissue of Diet-Induced Obese Mice

Int J Mol Sci. 2018 Apr 6;19(4):1095. doi: 10.3390/ijms19041095.

Abstract

Consumption of a high-fat diet (HFD) promotes the development of obesity, a disease resulting from an imbalance between energy intake and energy expenditure. Brown adipose tissue (BAT) has thermogenic capacity that burns calories to produce heat, and it is a potential target for the treatment and prevention of obesity. There is limited information regarding the impact of HFD on the BAT transcriptome. We hypothesized that HFD-induced obesity would lead to transcriptional regulation of BAT genes. RNA sequencing was used to generate global transcriptome profiles from BAT of lean mice fed with a low-fat diet (LFD) and obese mice fed with a HFD. Gene Ontology (GO) analysis identified increased expression of genes involved in biological processes (BP) related to immune responses, which enhanced molecular function (MF) in chemokine activity; decreased expression of genes involved in BP related to ion transport and muscle structure development, which reduced MF in channel and transporter activity and structural binding. Kyoto Encyclopedia of Genes and Genomes (KEGG) functional pathway analysis indicated that pathways associated with innate immunity were enhanced by HFD, while pathways associated with muscle contraction and calcium signaling were suppressed by HFD. Collectively, these results suggest that diet-induced obesity changes transcriptomic signatures of BAT, leading to dysfunction involving inflammation, calcium signaling, ion transport, and cell structural development.

Keywords: RNA sequencing; brown adipose tissue; calcium signaling; high-fat diet; inflammation; ion transport; muscle system process.

MeSH terms

  • Adipose Tissue, Brown / metabolism*
  • Animals
  • Diet, High-Fat / adverse effects
  • Gene Expression Profiling
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Obesity / etiology
  • Obesity / genetics*
  • Obesity / metabolism
  • Transcriptome*