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Association between 5-hydroxytryptamine release and insulin secretion.

E Gylfe

    The Journal of Endocrinology
    |August 1, 1978
    PubMed
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    Glucose stimulates serotonin release from pancreatic beta-cells, particularly when combined with IBMX. This efflux, primarily 5-hydroxytryptamine (5-HT), suggests exocytotic release linked to insulin secretion.

    Area of Science:

    • Biochemistry
    • Endocrinology
    • Cell Biology

    Background:

    • Pancreatic beta-cells are central to glucose homeostasis and insulin secretion.
    • Serotonin (5-HT) plays a role in various physiological processes, including potential paracrine signaling within islets.
    • Understanding the mechanisms of 5-HT release from beta-cells is crucial for metabolic research.

    Purpose of the Study:

    • To investigate the efflux of serotonin (5-HT) from pancreatic beta-cells in response to glucose stimulation.
    • To explore the role of phosphodiesterase inhibition and calcium in modulating 5-HT release.
    • To determine if 5-HT release is linked to insulin secretion mechanisms.

    Main Methods:

    • Perifusion of beta-cell-rich pancreatic islets from ob/ob mice loaded with radiolabeled 5-HT or 5-HTP.

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  • Varying glucose concentrations (3-20 mmol/l) in the perifusion medium.
  • Addition of phosphodiesterase inhibitor (IBMX) and manipulation of calcium levels or adrenaline presence.

    • Main Results:

    • Over 90% of radioactivity was released as [3H]5-HT after loading with [3H]5-HTP.
    • Glucose (20 mmol/l) enhanced 5-HT efflux in islets from fed mice, potentiated by IBMX.
    • Glucose-stimulated efflux was reduced by calcium omission or adrenaline, and required IBMX in starved mice.

    Conclusions:

    • Glucose stimulates the efflux of 5-HT from pancreatic beta-cells, suggesting a link to insulin secretion.
    • Exocytotic release is a likely mechanism, though basal non-exocytotic transport also occurs.
    • The findings support a role for 5-HT in beta-cell function and glucose regulation.