2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced impairment of glucose-stimulated insulin secretion in isolated rat pancreatic islets

Novelli, Michela; Piaggi, Simona; Tata, Vincenzo De

doi:10.1016/j.toxlet.2004.12.004

Cited by 69 publications

(67 citation statements)

References 47 publications

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“…The second phase response begins when glucose levels increase slowly and progressively for up to 4 h [35] . As in many other studies, we measured the insulin release over 60 min in static culture after incubating in low (2.8 mmol/L) and then high (16.7 mmol/L) glucose concentrations [19,20,36] . Therefore, the effect of fentanyl on glucose-stimulated insulin release in rat islets in dynamic culture also needs to be investigated.…”

Section: Discussionmentioning

confidence: 99%

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Fentanyl inhibits glucose-stimulated insulin release from β-cells in rat pancreatic islets

Qian¹,

Wang²,

Liu³

et al. 2009

WJG

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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.

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Section: Discussionmentioning

confidence: 99%

“…Supernatant from each well was collected and the insulin level was determined using a rat insulin radioimmunoassay kit (Linco Research, Inc, St Charles, MO, USA). The stimulation index (SI) was calculated by dividing the value of high glucosestimulated secretion by the value of low glucosestimulated secretion [19,20] .…”

Section: Islet Viabilitymentioning

confidence: 99%

Fentanyl inhibits glucose-stimulated insulin release from β-cells in rat pancreatic islets

Qian¹,

Wang²,

Liu³

et al. 2009

WJG

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“…Several hormone systems in different cell types and tissues and at different developmental stages are being altered by dioxin [74], leading to a complex disruption of multiple endocrine systems. One of the most common symptoms seen in animal species after TCDD exposure is loss of body weight or reduced weight gain [75], commonly referred to as wasting syndrome [76]. Since hypophagia, hyperlipidaemia and hypertriglyceridaemia are observed in TCDD-induced alterations in body weight, the assumption is made that affected animals are unable to utilise the energy-rich nutritional compounds available in their blood.…”

Section: Popsmentioning

confidence: 99%

“…Since hypophagia, hyperlipidaemia and hypertriglyceridaemia are observed in TCDD-induced alterations in body weight, the assumption is made that affected animals are unable to utilise the energy-rich nutritional compounds available in their blood. Metabolic derangements related to glucose metabolism have been considered to play a crucial role in the induction of this wasting syndrome [75]. The most important reported effects of TCDD on glucose homeostasis are the reduction of glucose uptake by adipose tissue, liver and pancreas (in vivo as well as in vitro) [77,78], accompanied by decreased insulin production and secretion by the pancreatic beta cells [79].…”

Section: Popsmentioning

confidence: 99%

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Environmental pollutants and type 2 diabetes: a review of mechanisms that can disrupt beta cell function

et al. 2011

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The prevalence of diabetes mellitus is currently at epidemic proportions and it is estimated that it will increase even further over the next decades. Although genetic predisposition and lifestyle choices are commonly accepted reasons for the occurrence of type 2 diabetes, it has recently been suggested that environmental pollutants are additional risk factors for diabetes development and this review aims to give an overview of the current evidence for this. More specifically, because of the crucial role of pancreatic beta cells in the development and progression of type 2 diabetes, the present work summarises the known effects of several compounds on beta cell function with reference to mechanistic studies that have elucidated how these compounds interfere with the insulin secreting capacity of beta cells. Oestrogenic compounds, organophosphorus compounds, persistent organic pollutants and heavy metals are discussed, and a critical reflection on the relevance of the concentrations used in mechanistic studies relative to the levels found in the human population is given. It is clear that some environmental pollutants affect pancreatic beta cell function, as both epidemiological and experimental research is accumulating. This supports the need to develop a solid and structured platform to fully explore the diabetes-inducing potential of pollutants.

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Role of the AHR and its Structure in TCDD Toxicity

Pohjanvirta

Korkalainen

Moffat

et al. 2011

The AH Receptor in Biology and Toxicology

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2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced impairment of glucose-stimulated insulin secretion in isolated rat pancreatic islets

Cited by 69 publications

References 47 publications

Fentanyl inhibits glucose-stimulated insulin release from β-cells in rat pancreatic islets

Fentanyl inhibits glucose-stimulated insulin release from β-cells in rat pancreatic islets

Environmental pollutants and type 2 diabetes: a review of mechanisms that can disrupt beta cell function

Role of the AHR and its Structure in TCDD Toxicity

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