AIM: To explore the effects of fentanyl on insulin release from freshly isolated rat pancreatic islets in static culture.METHODS: Islets were isolated from the pancreas of mature Sprague Dawley rats by common bile duct intraductal collagenase V digestion and were purified by discontinuous Ficoll density gradient centrifugation. The islets were divided into four groups according to the fentanyl concentration: control group (0 ng/mL), group -□(0.3 ng/mL), group□(3.0 ng/mL), and group□(30 ng/mL). In each group, the islets were co-cultured for 48 h with drugs under static conditions with fentanyl alone, fentanyl + 0.1 μg/mL naloxone or fentanyl + 1.0 μg/mL naloxone. Cell viability was assessed by the MTT assay. Insulin release in response to low and high concentrations (2.8 mmol/L and 16.7 mmol/L, respectively) of glucose was investigated and electron microscopy morphological assessment was performed.RESULTS: Low-and high-glucose-stimulated insulin release in the control group was significantly higherthan in groups□and□(62.33 ± 9.67 μIU vs 47.75 ±8.47 μIU, 39.67 ± 6.18 μIU and 125.5 ± 22.04 μIU vs 96.17 ± 14.17 μIU, 75.17 ± 13.57 μIU, respectively, P <0.01) and was lowest in group □(P < 0.01). After adding1 μg/mL naloxone, insulin release in groups □and□wasnot different from the control group. Electron microscopy studies showed that the islets were damaged by 30 ng/mL fentanyl.CONCLUSION: Fentanyl inhibited glucose-stimulated insulin release from rat islets, which could be prevented by naloxone. Higher concentrations of fentanyl significantly damaged β-cells of rat islets. AIM: To explore the effects of fentanyl on insulin release from freshly isolated rat pancreatic islets in static culture. METHODS: Islets were isolated from the pancreas of mature Sprague Dawley rats by common bile duct intraductal collagenase V digestion and were purified by a discontinuous Ficoll density gradient centrifugation. The islets were divided into four groups according to the fentanyl concentration: control group (0 ng / mL), group - □ (0.3 ng / mL), group □ mL). In each group, the islets were co-cultured for 48 h with drugs under static conditions with fentanyl alone, fentanyl + 0.1 μg / mL naloxone or fentanyl + 1.0 μg / mL naloxone. Cell viability was assessed by the MTT assay. Insulin release in response to low and high concentrations (2.8 mmol / L and 16.7 mmol / L, respectively) of glucose was investigated and electron microscopy morphological assessment was performed .RESULTS: Low-and high-glucose-stimulated insulin release in the control group was significantly higherthan in groups □ and □ (62.33 ± 9.67 μIU vs 47.75 ± 8.47 μIU, 39.67 ± 6.18 μIU and 125.5 ± 22.04 μIU vs 96.17 ± 14.17 μIU, 75.17 ± 13.57 μIU, respectively, P <0.01) and was lowest in group □ (P <0.01). After adding 1 μg / mL naloxone, insulin release in groups □ and □ was not different from the control group. Electron microscopy showed showed the islets were damaged by 30 ng / mL fentanyl.CONCLUSION: Fentanyl inhibited glucose-stimulated insulin concentrations from rat islets, which could be prevented by naloxone. Higher concentrations of fentanyl significantly damaged β-cells of rat islets.