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Updated: May 22, 2026
12:12
Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
Published on: June 16, 2011
Pentamidine-induced beta cell toxicity is not preventable by high glucose
The American Journal of the Medical Sciences
|August 1, 1989
Summary
Pentamidine treatment for pneumocystis pneumonia can damage beta cells, leading to irreversible insulin secretion defects. Glucose does not prevent this pentamidine-induced beta cell damage in vitro.
Area of Science:
- Endocrinology
- Pharmacology
- Cell Biology
Background:
- The AIDS epidemic has increased the use of pentamidine for pneumocystis pneumonia.
- Pentamidine treatment is associated with an increasing incidence of beta cell damage.
Purpose of the Study:
- To investigate the in vitro effects of pentamidine on beta cell function.
- To determine if glucose can prevent pentamidine-induced beta cell toxicity.
Main Methods:
- Perfused rat islets were used to measure insulin secretion as an indicator of beta cell damage.
- Islets were incubated with or without pentamidine (10^-6 M) in a medium with 100 mg/dl glucose.
- Insulin secretory responses to low (60 mg/dl) and high (300 mg/dl) glucose were assessed.
Main Results:
- Pentamidine incubation caused basal hypersecretion of insulin and completely abolished the glucose-stimulated insulin secretion.
- Coincubation with high glucose concentrations did not prevent these secretory defects.
- Extended culture of pentamidine-treated islets did not restore insulin secretion, indicating irreversible damage.
Conclusions:
- Pentamidine induces irreversible beta cell damage.
- High glucose concentrations do not protect against pentamidine-induced beta cell toxicity.
- The mechanism of pentamidine-induced beta cell damage may differ from that of alloxan.
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