Pentamidine–Induced Beta Cell Toxicity Is Not Preventable by High Glucose

• Published in: The American journal of the medical sciences 1989-08, Vol.298 (2), p.89-92
• Main Authors: Zhou, Dao Biao, Ipp, Eli
• Format: Article
• Language: English
• Subjects: Amidines - toxicity; Animals; Biological and medical sciences; Diabetes; Drug toxicity and drugs side effects treatment; Glucose - therapeutic use; In Vitro Techniques; Insulin; Insulin - metabolism; Insulin Secretion; Islets Of Langerhans; Islets of Langerhans - drug effects; Islets of Langerhans - metabolism; Male; Medical sciences; Pentamidine; Pentamidine - toxicity; Pharmacology. Drug treatments; Rats; Rats, Inbred Strains; Toxicity: digestive system
• ISSN: 0002-9629; 1538-2990
• DOI: 10.1097/00000441-198908000-00004

The incidence of beta cell damage attributable to pentamidine treatment of pneumocystis pneumonia is increasing in frequency because of the AIDS epidemic. We carried out in vitro studies in perfused rat islets using insulin secretion as an index of beta cell damage to study the effects of pentamidine and to test whether glucose can prevent toxicity in this physiologic model. Isolated islets were cultured for 16—18 hours of static incubation, in a culture medium containing 100 mg/dl glucose, with or without pentamidine (10−6 M, a therapeutic concentration). Islets were then perfused with media containing 60 mg/dl followed by 300 mg/dl glucose concentrations to study the insulin secretory response. Incubation of islets with pentamidine was associated with subsequent basal hypersecretion of insulin (0.40 ± 0.05 μU/islet.5 minute vs. 0.18 ± 0.04 μU/islet.5 minute, p