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The inexhaustible beta cell.

A I Vinik, W J Kalk, J L Botha

    Diabetes
    |January 1, 1976
    PubMed
    Summary
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    Intensive stimulation of pancreatic beta-cells produced significant insulin release in all groups. Mild diabetics showed an exaggerated response, while severe diabetics and pancreatitis patients had a reduced insulin output.

    Area of Science:

    • Endocrinology
    • Metabolic Research
    • Diabetes Mellitus Research

    Background:

    • Pancreatic beta-cell function is crucial for glucose homeostasis.
    • Understanding beta-cell response to stimuli is key in diabetes and pancreatitis.
    • Maturity-onset diabetes and chronic pancreatitis affect beta-cell function.

    Purpose of the Study:

    • To investigate the insulin secretory response of pancreatic beta-cells to repeated intensive stimulation.
    • To compare beta-cell function in normal individuals, mild to severe diabetics, and chronic pancreatitis patients.

    Main Methods:

    • 42 subjects (22 controls, 10 mild-severe diabetics, 10 pancreatitis patients) underwent stimulation.
    • Stimulation involved repeated oral glucose (75 gm) and intravenous glucagon (1 mg) plus tolbutamide (0.5 gm).

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  • Insulin release and blood glucose levels were monitored.
  • Main Results:

    • All groups exhibited marked insulin release spikes following combined stimuli.
    • Total calculated insulin output was comparable to normal daily output across groups.
    • Severe diabetics and pancreatitis patients showed quantitatively smaller insulin responses.
    • Mild diabetics exhibited an exaggerated response to the second oral glucose dose, suggesting enteroinsular axis overactivity.
    • No hypoglycemia occurred despite high insulin levels.

    Conclusions:

    • Pancreatic beta-cells can be stimulated to release significant insulin, even in diabetic and pancreatitis conditions.
    • Quantitative differences in insulin response exist between normal, mild diabetic, severe diabetic, and pancreatitis groups.
    • The enteroinsular axis may be overactive in mild diabetes.
    • Intensive stimulation protocols can reveal functional reserve and differences in beta-cell response without inducing hypoglycemia.