Russell's viper venom stimulates insulin secretion from rat islets of Langerhans
Autor: | Peter B. Jones, F. M. Mann |
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Rok vydání: | 1993 |
Předmět: |
medicine.medical_specialty
Endocrinology Diabetes and Metabolism medicine.medical_treatment Stimulation Viper Venoms Phospholipases A Islets of Langerhans Endocrinology Phospholipase A2 Internal medicine medicine Extracellular Animals Insulin Secretion Cells Cultured Protein Kinase C Protein kinase C Pancreatic hormone geography geography.geographical_feature_category biology Islet Stimulation Chemical Rats Phospholipases A2 Quinacrine biology.protein Calcium |
Zdroj: | Journal of Endocrinology. 136:27-33 |
ISSN: | 1479-6805 0022-0795 |
DOI: | 10.1677/joe.0.1360027 |
Popis: | Burmese Russell's viper venom (RVV) caused a dose-and temperature-dependent stimulation of insulin secretion from islets of Langerhans isolated from rat pancreas by collagenase digestion. RVV stimulated both basal and glucose-induced insulin secretion at concentrations which did not compromise islet cell viability as assessed by exclusion of trypan blue dye. The effects of RVV on insulin secretion could not be attributed to the activation of protein kinase C (PKC), since down-regulation of PKC by prolonged exposure to a tumour-promoting phorbol ester did not abolish subsequent secretory responses to RVV. However, RVV-induced insulin secretion was inhibited in the absence of extracellular Ca2 +, and RVV did not stimulate insulin secretion from Ca2+-clamped electrically permeabilized islets at either substimulatory (50 nmol/l) or stimulatory (10 μmol/l) concentrations of Ca2 +, suggesting that changes in cytosolic Ca2+ are important in the stimulation of insulin secretion by RVV. The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion. Journal of Endocrinology (1993) 136, 27–33 |
Databáze: | OpenAIRE |
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