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Preserved pulsatile insulin release from prediabetic mouse islets.

J M Lin1, J Sternesjö, S Sandler

  • 1Department of Medical Cell Biology, Uppsala University, Sweden.

Endocrinology
|August 28, 1999
PubMed
Summary
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Type I diabetes disrupts insulin release patterns. In nonobese diabetic mice, islet cell infiltration reduces insulin pulse amplitude, not pulsatility, suggesting amplitude is key to diabetes-related insulin changes.

Area of Science:

  • Endocrinology
  • Immunology
  • Metabolic Disorders

Background:

  • Type I diabetes is characterized by altered plasma insulin patterns.
  • Islet secretory patterns are implicated in these changes.
  • Nonobese diabetic (NOD) mice serve as a model for type I diabetes.

Purpose of the Study:

  • To investigate insulin release patterns from NOD mouse islets at different ages.
  • To determine the impact of islet infiltration on insulin secretion.
  • To explore potential mechanisms behind altered insulin patterns in type I diabetes.

Main Methods:

  • Isolating islets from NOD mice at 5, 13, and 25 weeks of age.
  • Measuring insulin release in response to glucose concentration changes (3-11 mM).
  • Assessing glucose oxidation rates and insulin pulsatility.

Related Experiment Videos

  • Culturing infiltrated islets to observe effects on cell infiltration and function.

    • Main Results:

    • Islets from young NOD mice (5 weeks) showed robust, pulsatile insulin release with glucose increase.
    • Islets from older NOD mice (13, 25 weeks) exhibited reduced glucose-induced insulin release despite maintained pulsatility.
    • Reduced glucose oxidation was observed in infiltrated islets.
    • Islet culture normalized glucose oxidation and insulin release.
    • Mitochondrial substrate stimulation revealed similar insulin pulse amplitudes in control and infiltrated islets.

    Conclusions:

    • The deranged plasma insulin pattern in type I diabetes may stem from decreased insulin pulse amplitude.
    • Loss of pulsatile insulin release is less likely the primary cause.
    • Islet infiltration and impaired glucose metabolism contribute to reduced insulin pulse amplitude.