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FA1 Induces Pro-Inflammatory and Anti-Adipogenic Pathways/Markers in Human Myotubes Established from Lean, Obese, and

Basem M Abdallah1, Henning Beck-Nielsen, Michael Gaster

  • 1Molecular Endocrinology Laboratory (KMEB), Odense University Hospital, University of Southern Denmark Odense, Denmark.

Frontiers in Endocrinology
|April 12, 2013
PubMed
Abstract

Insights

Delta like 1/fetal antigen 1 (Dlk1/FA1) does not directly impact glucose or lipid metabolism in human myotubes. Instead, FA1 promotes inflammation and inhibits adipogenesis, potentially contributing to insulin resistance.

Area of Science:

  • Endocrinology
  • Metabolic research
  • Cell biology

Background:

  • Delta like 1/fetal antigen 1 (Dlk1/FA1) is a secreted protein known to inhibit adipogenesis.
  • Previous studies suggest Dlk1/FA1 induces insulin resistance in mice.
  • The role of circulating Dlk1/FA1 in human insulin resistance and type 2 diabetes requires further investigation.

Purpose of the Study:

  • To investigate the involvement of circulating Dlk1/FA1 in insulin resistance and type 2 diabetes in human subjects.
  • To study the effects of chronic FA1 on intermediary metabolism in human myotubes from lean, obese, and type 2 diabetic individuals.

Main Methods:

  • Myotube cultures were established from lean, obese, and type 2 diabetic (T2D) subjects.
  • Cultures were treated with soluble FA1 with or without palmitate (PA).
  • Glucose and lipid metabolism were assessed using labeled precursors; gene expression was analyzed via real-time PCR.

Main Results:

  • Diabetic myotubes showed reduced insulin-stimulated glucose metabolism and basal PA oxidation compared to lean myotubes.
  • Chronic FA1 exposure did not directly affect intermediary metabolism in any group.
  • FA1 induced pro-inflammatory cytokines (IL-6, CCL2) and reduced adipogenic markers, inhibiting myotube differentiation into adipocytes.

Conclusions:

  • FA1 does not directly impact glucose and lipid metabolism in human myotubes.
  • FA1-induced insulin resistance may be primarily mediated by pro-inflammatory cytokine stimulation, which subsequently inhibits adipogenesis.
Keywords:
Dlk1FA1Pref-1human myotubesinsulin resistanceobesityskeletal muscletype 2 diabetes

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