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Updated: Jul 28, 2025

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
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Sulfatide inhibits fibroblast growth, activation and oxidative stress induced by ectopic insulin

Allan Roeske-Nielsen1, Jan-Eric Månsson2,3, Hasim Tekin1

  • 1Bartholin Instituttet, Rigshospitalet, Copenhagen, Denmark.

Diabetes, Obesity & Metabolism
|May 29, 2023
PubMed
Abstract

Insights

Sulfatide significantly inhibits human fibroblast growth, offering a potential therapeutic addition to insulin formulations for diabetes patients. This could reduce adverse effects and enhance patient well-being.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Fibroblast proliferation is crucial for tissue repair but can be dysregulated.
  • Insulin and related growth factors stimulate fibroblast activity.
  • Sulfatides are sphingolipids with diverse cellular roles.

Purpose of the Study:

  • To investigate the impact of sulfatide on human primary fibroblast gene expression and proliferation.
  • To assess sulfatide's effects in conjunction with insulin and other growth factors.

Main Methods:

  • Human primary fibroblasts were treated with varying concentrations of sulfatide and galactosylceramide (GalCer).
  • Proliferation was measured using 3H-thymidine incorporation.
  • Gene expression profiling was performed using microarray analysis.

Main Results:

  • Sulfatide and GalCer inhibited fibroblast growth by 32%-82% when combined with insulin.
  • Sulfatide reduced membrane leakage following hydrogen peroxide challenge.
  • Gene expression analysis revealed alterations in cell cycle, TGF-β signaling, and intracellular signaling pathways, including a 2-fold decrease in NFKBIA.

Conclusions:

  • Sulfatide demonstrates a potent inhibitory effect on fibroblast proliferation.
  • The addition of sulfatide to insulin formulations may mitigate adverse fibroblast proliferation in diabetic patients.
  • This approach could improve patient outcomes and well-being.
Keywords:
beta cell devicesfibroblastssphingolipidssulfatidetype 1 diabetes

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