MSC attenuate diabetes-induced functional impairment in adipocytes via secretion of insulin-like growth factor-1

Biochem Biophys Res Commun. 2014 Sep 12;452(1):99-105. doi: 10.1016/j.bbrc.2014.08.060. Epub 2014 Aug 21.

Abstract

The function of subcutaneous adipocytes in promoting wound healing is significantly suppressed in diabetic wounds. Recent studies have demonstrated the ability of mesenchymal stem cell (MSC) to ameliorate impaired diabetic wound healing. We hypothesized that MSC function may involve subcutaneous adipocytes. The abnormal function of subcutaneous adipocytes from STZ induced diabetic mice including glucose uptake and free fatty acid (FFA) secretion level were assessed. Then these cells were co-cultured with MSC via a transwell system to observe the changes of metabolic index and glucose transporter four (GLUT4) as well as phosphoinositide 3-kinase/protein kinase (PI3K/AKT) signaling pathway expression. The results of metabolic index suggest that MSC obviously attenuated the diabetes-induced functional impairment. Both mRNA and protein expression analyses showed that PI3K/AKT insulin signaling pathway and GLUT4 expression were up-regulated. These changes were substantially associated with a increased level of insulin-like growth factor-1 (IGF-1) secretion from MSC. These findings suggest that MSC could attenuate abnormal function of diabetic adipocytes by IGF-1secretion, which was more or less associated with the beneficial effects of MSC on improving diabetic wound healing.

Keywords: Adipocytes; Conditioned medium (CM); IGF-1; MSC; Wound.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / metabolism
  • Adipocytes / pathology*
  • Animals
  • Base Sequence
  • Cells, Cultured
  • DNA Primers
  • Diabetes Mellitus, Experimental / metabolism
  • Diabetes Mellitus, Experimental / pathology*
  • Insulin / metabolism
  • Insulin-Like Growth Factor I / metabolism*
  • Male
  • Mesenchymal Stem Cells / cytology*
  • Mice
  • Mice, Inbred C57BL
  • Real-Time Polymerase Chain Reaction
  • Signal Transduction
  • Streptozocin

Substances

  • DNA Primers
  • Insulin
  • Streptozocin
  • Insulin-Like Growth Factor I