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Decrease in insulin-containing secretory granules and mitochondrial gene expression in mouse pancreatic islets
J E Moreira1, A R Hand, L A Håkan Borg
1Clinical Investigation and Patient Care Branch, National Institute of Dental Research, National Institute of Health, Bethesda 20892.
Virchows Archiv. B, Cell Pathology Including Molecular Pathology
|January 1, 1991
Summary
Streptozotocin (SZ) exposure in mouse islets impairs insulin secretion and reduces cytochrome b mRNA, suggesting damage to mitochondrial DNA. This impacts beta-cell function without causing lasting mitochondrial damage.
Area of Science:
- Endocrinology
- Cell Biology
- Mitochondrial Biology
Background:
- Streptozotocin (SZ) exposure in vitro reduces pancreatic islet secretory response.
- This impairment is linked to altered mitochondrial substrate metabolism.
Purpose of the Study:
- To investigate the long-term effects of SZ on pancreatic beta-cell structure and function.
- To clarify the impact of SZ on mitochondrial integrity and gene expression.
Main Methods:
- In vitro exposure of mouse pancreatic islets to streptozotocin (SZ).
- Ultrastructural analysis and morphometric assessment of beta-cells.
- Dot-blot analysis to evaluate mitochondrial DNA-encoded cytochrome b mRNA levels.
Main Results:
- SZ induced ultrastructural changes in endoplasmic reticulum and Golgi at 4 hours.
- Beta-cells showed preserved structure but reduced insulin granules 2-6 days post-exposure.
- Mitochondrial volume fraction remained normal, but cytochrome b mRNA decreased significantly.
Conclusions:
- SZ treatment does not cause lasting mitochondrial ultrastructural damage.
- A decrease in cytochrome b mRNA suggests SZ can induce damage to mitochondrial DNA.
- Impaired beta-cell function following SZ is associated with mitochondrial DNA alterations.