Interleukin-6 increases insulin-stimulated glucose disposal in humans and glucose uptake and fatty acid oxidation in vitro via AMP-activated protein kinase

Diabetes. 2006 Oct;55(10):2688-97. doi: 10.2337/db05-1404.

Abstract

Although interleukin-6 (IL-6) has been associated with insulin resistance, little is known regarding the effects of IL-6 on insulin sensitivity in humans in vivo. Here, we show that IL-6 infusion increases glucose disposal without affecting the complete suppression of endogenous glucose production during a hyperinsulinemic-euglycemic clamp in healthy humans. Because skeletal muscle accounts for most of the insulin-stimulated glucose disposal in vivo, we examined the mechanism(s) by which IL-6 may affect muscle metabolism using L6 myotubes. IL-6 treatment increased fatty acid oxidation, basal and insulin-stimulated glucose uptake, and translocation of GLUT4 to the plasma membrane. Furthermore, IL-6 rapidly and markedly increased AMP-activated protein kinase (AMPK). To determine whether the activation of AMPK mediated cellular metabolic events, we conducted experiments using L6 myotubes infected with dominant-negative AMPK alpha-subunit. The effects described above were abrogated in AMPK dominant-negative-infected cells. Our results demonstrate that acute IL-6 treatment enhances insulin-stimulated glucose disposal in humans in vivo, while the effects of IL-6 on glucose and fatty acid metabolism in vitro appear to be mediated by AMPK.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • AMP-Activated Protein Kinases
  • Adult
  • Aminoimidazole Carboxamide / analogs & derivatives
  • Aminoimidazole Carboxamide / pharmacology
  • Animals
  • Cell Line
  • Cell Membrane / metabolism
  • Fatty Acids / metabolism*
  • Glucose / metabolism*
  • Glucose Clamp Technique
  • Glucose Transporter Type 4
  • Humans
  • Hyperinsulinism / physiopathology
  • Insulin / physiology*
  • Interleukin-6 / pharmacology*
  • Interleukin-6 / physiology
  • Male
  • Mice
  • Mice, Knockout
  • Multienzyme Complexes / metabolism*
  • Myoblasts
  • Protein Serine-Threonine Kinases / metabolism*
  • Rats
  • Recombinant Proteins / pharmacology
  • Ribonucleotides / pharmacology
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / drug effects
  • Suppressor of Cytokine Signaling 3 Protein
  • Suppressor of Cytokine Signaling Proteins / metabolism

Substances

  • Fatty Acids
  • Glucose Transporter Type 4
  • Insulin
  • Interleukin-6
  • Multienzyme Complexes
  • Recombinant Proteins
  • Ribonucleotides
  • STAT3 Transcription Factor
  • Slc2a4 protein, rat
  • Socs3 protein, rat
  • Stat3 protein, rat
  • Suppressor of Cytokine Signaling 3 Protein
  • Suppressor of Cytokine Signaling Proteins
  • Aminoimidazole Carboxamide
  • Protein Serine-Threonine Kinases
  • AMP-Activated Protein Kinases
  • AICA ribonucleotide
  • Glucose