The Impact of Psilocybin on High Glucose/Lipid-Induced Changes in INS-1 Cell Viability and Dedifferentiation
Genes – January 29, 2024
Source: OpenAlex
Summary
A potent hallucinogen, psilocybin, significantly protects pancreatic cells. In cell biology experiments using an INS-1 832/13 rat insulinoma cell line, psilocybin pretreatment reduced β-cell loss and dedifferentiation under high glucose-high lipid conditions. This chemistry, acting on serotonin receptors, modulated apoptotic biomarkers and key genes, improving cell viability. These biological insights, part of broader Psychedelics and Drug Studies, highlight psilocybin's potential for pancreatic function and diabetes intervention, suggesting new avenues for drug development.
Abstract
Serotonin emerges as a pivotal factor influencing the growth and functionality of β-cells. Psilocybin, a natural compound derived from mushrooms of the Psilocybe genus, exerts agonistic effects on the serotonin 5-HT2A and 5-HT2B receptors, thereby mimicking serotonin’s behavior. This study investigates the potential impacts of psilocybin on β-cell viability, dedifferentiation, and function using an in vitro system. The INS-1 832/13 Rat Insulinoma cell line underwent psilocybin pretreatment, followed by exposure to high glucose-high lipid (HG-HL) conditions for specific time periods. After being harvested from treated cells, total transcript and cellular protein were utilized for further investigation. Our findings implied that psilocybin administration effectively mitigates HG-HL-stimulated β-cell loss, potentially mediated through the modulation of apoptotic biomarkers, which is possibly related to the mitigation of TXNIP, STAT-1, and STAT-3 phosphorylation. Furthermore, psilocybin exhibits the capacity to modulate the expression of key genes associated with β-cell dedifferentiation, including Pou5f1 and Nanog, indicating its potential in attenuating β-cell dedifferentiation. This research lays the groundwork for further exploration into the therapeutic potential of psilocybin in Type II diabetes intervention.