ArticleDiabetologia2013
NADPH oxidase inhibition prevents beta cell dysfunction induced by prolonged elevation of oleate in rodents.
Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Expression, localization and regulation of NADPH oxidases in pancreatic beta cells.Redox report : communications in free radical research · 2025Article
- β-Cell Insulin Resistance Plays a Causal Role in Fat-Induced β-Cell Dysfunction In Vitro and In Vivo.Endocrinology · 2024Article
- Hypoxia in Aging and Aging-Related Diseases: Mechanism and Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Article
- 5-Bromoprotocatechualdehyde Combats against Palmitate Toxicity by Inhibiting Parkin Degradation and Reducing ROS-Induced Mitochondrial Damage in Pancreatic β-Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Review
- Pharmacologic or genetic activation of SIRT1 attenuates the fat-induced decrease in beta-cell function in vivo.Nutrition & diabetes · 2019Article
- Glucose-Induced β-Cell Dysfunction In Vivo: Evidence for a Causal Role of C-jun N-terminal Kinase Pathway.Endocrinology · 2018Article
- The Distinct Effects of Palmitic and Oleic Acid on Pancreatic Beta Cell Function: The Elucidation of Associated Mechanisms and Effector Molecules.Frontiers in pharmacology · 2018Article
- Effects of stevia on synaptic plasticity and NADPH oxidase level of CNS in conditions of metabolic disorders caused by fructose.BMC complementary and alternative medicine · 2017Article
- Chronic high fat feeding restricts islet mRNA translation initiation independently of ER stress via DNA damage and p53 activation.Scientific reports · 2017Article
- Rac1-NADPH oxidase signaling promotes CD36 activation under glucotoxic conditions in pancreatic beta cells.Redox biology · 2017Article
- Oxidative stress and calcium dysregulation by palmitate in type 2 diabetes.Experimental & molecular medicine · 2017Review
- Oxidative Stress in Pancreatic Beta Cell Regeneration.Oxidative medicine and cellular longevity · 2017Review
- Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity.Aging and disease · 2016Review
- Deprivation of L-Arginine Induces Oxidative Stress Mediated Apoptosis in Leishmania donovani Promastigotes: Contribution of the Polyamine Pathway.PLoS neglected tropical diseases · 2016Article
- Uncoupling protein-2 mediates the protective action of berberine against oxidative stress in rat insulinoma INS-1E cells and in diabetic mouse islets.British journal of pharmacology · 2014Article
- Lipotoxicity in the pancreatic beta cell: not just survival and function, but proliferation as well?Current diabetes reports · 2014Review
- Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
aims/hypothesisThe activation of NADPH oxidase has been implicated in NEFA-induced beta cell dysfunction. However, the causal role of this activation in vivo remains unclear. Here, using rodents, we investigated whether pharmacological or genetic inhibition of NADPH oxidase could prevent NEFA-induced beta cell dysfunction in vivo.
methodsNormal rats were infused for 48 h with saline or oleate with or without the NADPH oxidase inhibitor apocynin. In addition, NADPH oxidase subunit p47(phox)-null mice and wild-type littermate controls were infused with saline or oleate for 48 h. This was followed by measurement of NADPH oxidase activity, reactive oxygen species (ROS) and superoxide imaging and assessment of beta cell function in isolated islets and hyperglycaemic clamps.
resultsOleate infusion in rats increased NADPH oxidase activity, consistent with increased total but not mitochondrial superoxide in islets and impaired beta cell function in isolated islets and during hyperglycaemic clamps. Co-infusion of apocynin with oleate normalised NADPH oxidase activity and total superoxide levels and prevented beta cell dysfunction. Similarly, 48 h NEFA elevation in wild-type mice increased total but not mitochondrial superoxide and impaired beta cell function in isolated islets. p47(phox)-null mice were protected against these effects when subjected to 48 h oleate infusion. Finally, oleate increased the levels of total ROS, in both models, whereas inhibition of NADPH oxidase prevented this increase, suggesting that NADPH oxidase is the main source of ROS in this model. CONCLUSIONS/
interpretationThese data show that NADPH-oxidase-derived cytosolic superoxide is increased in islets upon oleate infusion in vivo; and whole-body NADPH-oxidase inhibition decreases superoxide in concert with restoration of islet function.
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