ArticleDiabetologia2011
Increased neuronal nitric oxide synthase dimerisation is involved in rat and human pancreatic beta cell hyperactivity in obesity.
Article in Diabetologia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- PIN (Protein Inhibitor of Neuronal Nitric Oxide Synthase) Modulates Glucose Uptake Through NO-Dependent and Independent Mechanisms in Rat Muscle Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- The Effect of Selected Nitric Oxide Synthase Polymorphisms on the Risk of Developing Diabetic Nephropathy.Antioxidants (Basel, Switzerland) · 2024Article
- β-Cell Heterogeneity and Plasticity.Advances in anatomy, embryology, and cell biology · 2024Review
- HIF-2α Preserves Mitochondrial Activity and Glucose Sensing in Compensating β-Cells in Obesity.Diabetes · 2022Article
- Review
- Human Nitric Oxide Synthase-Its Functions, Polymorphisms, and Inhibitors in the Context of Inflammation, Diabetes and Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- Nitric oxide signalling in the brain and its control of bodily functions.British journal of pharmacology · 2020Review
- Insulin secretion: The nitric oxide controversy.EXCLI journal · 2020Review
- Diet-induced obesity in young mice: Consequences on the pancreatic intrinsic nervous system control of insulin secretion.Endocrinology, diabetes & metabolism · 2020Article
- Actions of metformin and statins on lipid and glucose metabolism and possible benefit of combination therapy.Cardiovascular diabetology · 2018Review
- The Cells of the Islets of Langerhans.Journal of clinical medicine · 2018Review
- Human beta cell mass and function in diabetes: Recent advances in knowledge and technologies to understand disease pathogenesis.Molecular metabolism · 2017Review
- Article
- Similarity in Transcytosis of nNOSα in Enteric Nerve Terminals and Beta Cells of Pancreatic Islet.Frontiers in medicine · 2014Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisPancreatic beta cell hyperactivity is known to occur in obesity, particularly in insulin-resistant states. Our aim was to investigate whether changes in neuronal nitric oxide synthase (nNOS) function affect beta cell compensation in two relevant models: the Zucker fa/fa rats and pancreatic islets from obese humans.
methodsGlucose-induced insulin response was evaluated in the isolated perfused rat pancreas and in human pancreatic islets from obese individuals. Expression of nNOS (also known as NOS1) and subcellular localisation of nNOS were studied by quantitative RT-PCR, immunoblotting, immunofluorescence and electron microscopy.
resultsPancreatic beta cells from Zucker fa/fa rats and obese individuals were found to be hyper-responsive to glucose. Pharmacological blockade of nNOS was unable to modify beta cell response to glucose in fa/fa rats and in islets from obese individuals, suggesting an abnormal control of insulin secretion by the enzyme. In both cases, nNOS activity in islet cell extracts remained unchanged, despite a drastic increase in nNOS protein and an enhancement in the dimer/monomer ratio, pointing to the presence of high amounts of catalytically inactive enzyme. This relative decrease in activity could be mainly related to increases in islet asymmetric dimethyl-arginine content, an endogenous inhibitor of nNOS activity. In addition, mitochondrial nNOS level was decreased, which contrasts with a strongly increased association with insulin granules. CONCLUSIONS/
interpretationIncreased nNOS production and dimerisation, together with a relative decrease in catalytic activity and relocalisation, are involved in beta cell hyperactivity in insulin-resistant rats but also in human islets isolated from obese individuals.
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