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The Impact of Psilocybin on High Glucose/Lipid-Induced Changes in INS-1 Cell Viability and Dedifferentiation

Summary

Researchers tested whether psilocybin, a compound from magic mushrooms, could protect pancreatic β-cells (which produce insulin) from damage caused by high glucose and fat levels. Using laboratory cells, they found that psilocybin reduced β-cell death by preventing apoptosis and showed promise in reducing dedifferentiation (when cells lose their specialized functions). However, psilocybin didn’t restore the cells’ ability to respond to glucose by releasing insulin.

Background

Diabetes mellitus is a persistent metabolic disorder affecting over 537 million people globally. Pancreatic β-cell loss and dedifferentiation contribute to Type 2 diabetes development. Serotonin is a pivotal factor influencing β-cell growth and functionality, and psilocybin acts as an agonist on serotonin receptors.

Objective

This study investigates the potential impacts of psilocybin on β-cell viability, dedifferentiation, and function in high glucose/high lipid (HG-HL) conditions using INS-1 832/13 rat insulinoma cells.

Results

Psilocybin effectively mitigated HG-HL-induced β-cell loss by reducing apoptosis through modulation of TXNIP, STAT-1, and STAT-3 phosphorylation. Psilocybin downregulated dedifferentiation markers Pou5f1 and Nanog. However, psilocybin did not improve impaired glucose-stimulated insulin secretion under HG-HL conditions.

Conclusion

Psilocybin demonstrates therapeutic potential in protecting β-cells from HG-HL-induced loss through anti-apoptotic mechanisms and potential mitigation of β-cell dedifferentiation, laying groundwork for further exploration in Type 2 diabetes intervention.
  • Published in:Genes (Basel),
  • Study Type:In Vitro Experimental Study,
  • Source: 10.3390/genes15020183, PMID: 38397173
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