ArticleDiabetologia2003
Suppressive effects of a selective inducible nitric oxide synthase (iNOS) inhibitor on pancreatic beta-cell dysfunction.
Article in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 25 citations in OpenAlex.
- Effects of Black Cumin Seed Extract on Pancreatic Islet β-Cell Proliferation and Hypoglycemic Activity in Streptozotocin-Induced Diabetic Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Improving effect of combined inorganic nitrate and nitric oxide synthase inhibitor on pancreatic oxidative stress and impaired insulin secretion in streptozotocin induced-diabetic rats.Journal of diabetes and metabolic disorders · 2020Article
- Early Treatment with Empagliflozin and GABA ImprovesJournal of diabetes research · 2019Article
- Administration of heme arginate ameliorates murine type 2 diabetes independently of heme oxygenase activity.PloS one · 2013Article
- Inducible nitric-oxide synthase and nitric oxide donor decrease insulin receptor substrate-2 protein expression by promoting proteasome-dependent degradation in pancreatic beta-cells: involvement of glycogen synthase kinase-3beta.The Journal of biological chemistry · 2011Article
- Resveratrol prevents interleukin-1β-induced dysfunction of pancreatic β-cells.Journal of biomedical research · 2010Article
- Oxidative stress and beta-cell dysfunction.Pflugers Archiv : European journal of physiology · 2010Review
- Effects of renin-angiotensin system blockade on islet function in diabetic rats.Journal of endocrinological investigation · 2010Article
- IL-1beta receptor blockade protects islets against pro-inflammatory cytokine induced necrosis and apoptosis.Journal of cellular physiology · 2009Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisType 1 diabetes mellitus is an autoimmune disease characterized by dysfunction and destruction of the pancreatic beta cells. Interleukin-1beta (IL-1beta) has been reported to cause suppression of insulin secretion from pancreatic islets via induction of inducible nitric oxide synthase (iNOS) followed by nitric oxide (NO) production. In this study, we investigated the effects of inhibition of iNOS on pancreatic beta-cell dysfunction in non-obese diabetic (NOD) mice and IL-1beta-treated isolated rat pancreatic islets using a novel specific inhibitor, ONO-1714.
methodsFemale NOD mice which received subcutaneous infusion of ONO-1714 (4 microg/kg/day or 40 microg/kg/day) from 10 to 14 weeks after birth were compared with untreated NOD mice. In addition, pancreatic islets were isolated from Sprague-Dawley rats and cultured for 24 h with IL-1beta (100 U/mL) with or without ONO-1714 or the non-selective NOS inhibitor NG-monomethyl-L-arginine (L-NMMA). We measured insulin secretion and insulin content of the islets by ELISA, iNOS mRNA expression by reverse transcription-polymerase chain reaction, and NO generation by Griess Reagent System.
resultsHyperglycaemia was observed in NOD mice. ONO-1714 treatment blunted this increase and tended to preserve insulin secretion, although body weight increase did not differ between the groups. Insulitis was also attenuated in the ONO-1714-administered group compared to the control group. Furthermore, in isolated rat pancreatic islets ONO-1714 prevented IL-1beta-induced inhibition of insulin secretion, this protection being evident in much lower concentrations than with L-NMMA. While ONO-1714 completely inhibited IL-1beta-induced NO production, it did not reduce expression of islet iNOS mRNA. CONCLUSION/
interpretationThese findings indicate that ONO-1714 is promising as a therapeutic agent for autoimmune diabetes.
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