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Insulin release: the fuel hypothesis.

W J Malaisse, A Sener, A Herchuelz

    Metabolism: Clinical and Experimental
    |April 1, 1979
    PubMed
    Summary
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    Glucose metabolism in pancreatic B-cells triggers insulin release through specific ionic and metabolic events. Key factors like H+ and reduced pyridine nucleotides initiate this process, regulating fuel homeostasis.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Endocrinology

    Background:

    • Insulin release from pancreatic B-cells is directly regulated by circulating nutrients, primarily glucose.
    • The recognition of glucose as an insulinotropic agent is linked to metabolic changes within islet cells.
    • The precise coupling mechanism between metabolic shifts and subsequent ionic events remains under investigation.

    Purpose of the Study:

    • To elucidate the key coupling factors initiating glucose-stimulated insulin release.
    • To investigate the roles of H+ fluxes and reduced pyridine nucleotides in insulin secretion.
    • To explore the relationship between nutrient metabolism and hormonal release in pancreatic B-cells.

    Main Methods:

    • Analysis of metabolic changes within islet cells in response to glucose.

    Related Experiment Videos

  • Measurement of ionic fluxes (K+, Ca2+) and their correlation with nutrient levels.
  • Examination of reduced pyridine nucleotide (NAD(P)H) concentrations and their impact on ion transport.

    • Main Results:

    • H+ fluxes correlate with glucose-induced decreases in K+ and Ca2+ outflow, exhibiting hyperbolic dose-response curves.
    • Changes in NAD(P)H concentrations are linked to glucose-induced Ca2+ exchange, showing sigmoidal dose-response patterns similar to insulin release.
    • These findings suggest a critical role for H+ and NAD(P)H in mediating nutrient-stimulated insulin secretion.

    Conclusions:

    • The initiation of insulin release depends on the generation of H+ and reduced pyridine nucleotides.
    • A proposed coupling mechanism links metabolic nutrient utilization in islet cells to ionic events regulating insulin secretion.
    • This model provides insights into the regulation of fuel homeostasis and potential feedback mechanisms in pancreatic B-cells.