Stimulation of PAI-1 and adipokines by glucose in human adipose tissue in vitro

Biochem Biophys Res Commun. 2003 Oct 24;310(3):878-83. doi: 10.1016/j.bbrc.2003.09.091.

Abstract

Adipokines such as Plasminogen activator inhibitor-1 (PAI-1), interleukin (IL)-8, and tumor necrosis factor (TNF)-alpha are elevated in patients with obesity, insulin resistance, and type 2 diabetes. In the present study, we investigated whether glucose affected the production of these adipokines in human adipose tissue in vitro. Glucose (up to 35mM) increased secretion of PAI-1 (p<0.01) and IL-8 (p<0.01), but not TNF-alpha, in a dose- and time-dependent manner. Half-maximal stimulatory concentration of glucose was about 1mM. Glucosamine (5mM) decreased production of PAI-1 (p<0.05) and IL-8 (p<0.05), indicating that the hexosamine biosynthesis pathway is not involved in the glucose-induced increment in adipokine secretion. The present data demonstrate that glucose increases PAI-1 and IL-8 secretion. However, glucose concentrations above 5mM had no additional effects on adipokine secretion, suggesting that mechanisms other than diabetes/insulin resistance-related hyperglycemia may be involved in the observed elevation of these adipokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism*
  • Adult
  • Chemokines / metabolism*
  • Dose-Response Relationship, Drug
  • Female
  • Glucosamine / metabolism
  • Glucose / metabolism*
  • Glucose / pharmacology
  • Humans
  • Hyperglycemia / metabolism
  • In Vitro Techniques
  • Insulin / metabolism
  • Interleukin-8 / biosynthesis
  • Plasminogen Activator Inhibitor 1 / metabolism*
  • RNA, Messenger / metabolism
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Chemokines
  • Insulin
  • Interleukin-8
  • Plasminogen Activator Inhibitor 1
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Glucose
  • Glucosamine