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World J Gastroenterol. Sep 7, 2009; 15(33): 4163-4169
Published online Sep 7, 2009. doi: 10.3748/wjg.15.4163
Fentanyl inhibits glucose-stimulated insulin release from β-cells in rat pancreatic islets
Tao-Lai Qian, Xin-Hua Wang, Sheng Liu, Liang Ma, Ying Lu
Tao-Lai Qian, Xin-Hua Wang, Department of Pain Management, Shanghai East Hospital, Tongji University, Shanghai 200120, China
Sheng Liu, Department of Anesthesia, Shanghai East Hospital, Tongji University, Shanghai 200120, China
Liang Ma, Cell Therapy Center, Shanghai East Hospital, Tongji University, Shanghai 200120, China
Ying Lu, Central Laboratory, Shanghai East Hospital, Tongji University, Shanghai 200120, China
Author contributions: Qian TL was responsible for the review of the literature, the study design and initial preparation of the paper; Qian TL, Liu S and Ma L performed the majority of the experiments; Lu Y provided vital reagents and analytical tools and was also involved in editing the manuscript; Wang XH provided financial support for this work and prepared the final draft of the manuscript.
Correspondence to: Tao-Lai Qian, MD, Department of Pain Management, Shanghai East Hospital, Tongji University, 150 Jimo Road, Shanghai 2000120, China. qiantaolai@sina.com
Telephone: +86-21-38804518 Fax: +86-21-58798999
Received: April 22, 2009
Revised: July 7, 2009
Accepted: July 14, 2009
Published online: September 7, 2009
Abstract

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 I (0.3 ng/mL), group II (3.0 ng/mL), and group III (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 higher than in groups II and III (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 III (P < 0.01). After adding 1 μg/mL naloxone, insulin release in groups II and III was not 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.

Keywords: Fentanyl; Inhibition; Insulin release; Islets