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Related Experiment Videos

Stimulus-secretion coupling in beta-cells: modulation by pH.

C S Pace, J T Tarvin, J S Smith

    The American Journal of Physiology
    |January 1, 1983
    PubMed
    Summary
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    Changes in intracellular pH (pHi) significantly impact beta-cell electrical activity and insulin secretion. Lowering pHi enhances electrical spiking, while altering ion transport mechanisms affects secretory responses, revealing pH

    Area of Science:

    • Cellular physiology
    • Endocrinology
    • Ion transport

    Background:

    • Pancreatic beta-cells regulate glucose homeostasis through electrical activity and insulin secretion.
    • Intracellular and extracellular pH (pHi and pHo) are critical cellular parameters that can influence cell function.
    • The interplay between pH, glucose, and ion transport in beta-cells remains incompletely understood.

    Purpose of the Study:

    • To investigate the specific effects of altered pH on the electrical activity (EA) and secretory function of pancreatic beta-cells.
    • To elucidate the role of intracellular pH (pHi) versus extracellular pH (pHo) in modulating beta-cell responses.
    • To examine the impact of inhibiting specific ion transport systems (HCO3:Cl and Na:H antiports) on pH-mediated effects.

    Main Methods:

    Related Experiment Videos

  • Manipulating medium pH (pHo) and utilizing permeable weak buffers to alter intracellular pH (pHi) in beta-cells.
  • Recording electrical activity (EA) patterns, including depolarization and spike activity, under varying glucose and pH conditions.
  • Assessing the influence of specific inhibitors (DIDS, probenecid, amiloride) and ion concentrations ([Na+], HCO3-) on EA and 86Rb+ efflux (a marker for K+ permeability).
  • Measuring secretory responses in conjunction with electrical activity changes.

    • Main Results:

    • Decreased pHi, in the presence of glucose, induced sustained depolarization and spike activity, whereas increased pHi led to hyperpolarization or quiescence.
    • Inhibition of HCO3:Cl and Na:H antiports prolonged the active phase of electrical activity.
    • Alterations in pHi, not pHo, were found to induce effects on glucose-induced electrical and secretory events.
    • DIDS and amiloride enhanced glucose-induced EA but significantly inhibited the secretory response, indicating a dissociation between electrical and secretory pathways.

    Conclusions:

    • Intracellular pH (pHi) is a key modulator of glucose-induced electrical activity and cationic fluxes in pancreatic beta-cells.
    • Specific ion transport mechanisms (HCO3:Cl and Na:H antiports) play a role in pH-dependent regulation of beta-cell electrical activity.
    • There is a functional dissociation between the effects of pH modulators on beta-cell electrical activity and insulin secretion, suggesting complex regulatory pathways.