Glucose regulates RMI1 expression through the E2F pathways in adipose cells

Endocrine. 2011 Aug;40(1):56-61. doi: 10.1007/s12020-011-9455-4. Epub 2011 Mar 24.

Abstract

RecQ-mediated genome instability 1 (RMI1) has been identified as a novel energy homeostasis-related molecule. While recent studies have suggested that change in RMI1 expression levels in adipose tissue may affect the body's energy balance, no reports have identified the mechanism behind this expression regulation. In the present study, we found that RMI1 expression increased on differentiation of 3T3-L1 fibroblasts to adipocytes. In addition, glucose stimulation induced RMI1 expression to approximately eight times the baseline level. Further, knockdown of either E2F5 or E2F8 mRNA using siRNA suppressed this glucose-induced up-regulation of RMI1 expression. These results suggest that RMI1 expression may be regulated by glucose, at least in part, via E2F expression.

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / cytology
  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Adipose Tissue / cytology
  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism*
  • Animals
  • Carrier Proteins / metabolism*
  • Cell Differentiation / physiology
  • DNA-Binding Proteins
  • E2F Transcription Factors / drug effects
  • E2F Transcription Factors / genetics
  • E2F Transcription Factors / metabolism*
  • Fibroblasts / cytology
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Glucose / pharmacology*
  • Mice
  • Models, Animal
  • Nuclear Proteins / metabolism*
  • RNA, Messenger / metabolism
  • RNA, Small Interfering / pharmacology
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology*

Substances

  • Carrier Proteins
  • DNA-Binding Proteins
  • E2F Transcription Factors
  • Nuclear Proteins
  • RMI1 protein, mouse
  • RNA, Messenger
  • RNA, Small Interfering
  • Glucose