C-reactive protein inhibits high-molecular-weight adiponectin expression in 3T3-L1 adipocytes via PI3K/Akt pathway

Biochem Biophys Res Commun. 2016 Mar 25;472(1):19-25. doi: 10.1016/j.bbrc.2016.01.143. Epub 2016 Jan 23.

Abstract

Adiponectin, an adipose-specific protein hormone, is secreted from white adipose tissue and involved in glucose and lipid metabolism. It is assembled into low-molecular-weight trimer (LMW), middle-molecular-weight hexameric (MMW) and high-molecular-weight (HMW), among which HMW exhibits higher activity. In this study, we proved that C-reactive protein (CRP), an inflammatory marker, inhibited adiponectin expression, especially HMW in time-and dose-dependent manners. Furthermore, CRP decreased the HMW/total adiponectin ration and reduced adiponectin assembly by increasing ERp44, and decreasing Ero1-α and DsbA-L. CRP activated pAkt, the downstream of PI3K. Inhibition of PI3K or pAkt abolished the effect of CRP. Our study suggested that CRP decreased adiponectin expression and multimerization, while CRP-induced decline in adiponectin might be mediated through the PI3K/Akt pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Adiponectin / chemistry
  • Adiponectin / genetics
  • Adiponectin / metabolism*
  • Animals
  • C-Reactive Protein / metabolism*
  • C-Reactive Protein / pharmacology
  • Gene Expression
  • Inflammation Mediators / metabolism
  • Mice
  • Molecular Weight
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Protein Multimerization
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / drug effects

Substances

  • Adiponectin
  • Adipoq protein, mouse
  • Inflammation Mediators
  • C-Reactive Protein
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt