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Recherche transversale
(titres de publication, de périodique et noms de colloque inclus)
2017-09-25 - Article/Dans un journal avec peer-review - Anglais - 37 page(s)

Martin Blanche, Caron Nathalie, Jadot Ines, Colombaro V, Federici Gabrielle, Depommier Clara, Decleves Anne-Emilie , "Evaluation of iNOS inhibition on kidney function and structure in high-fat diet-induced kidney disease." in Experimental Physiology, 103, (1), 125-140, doi: 10.1113/EP086594

  • Edition : Cambridge University Press, Cambridge (United Kingdom)
  • Codes CREF : Sciences biomédicales (DI3200), Néphrologie - urologie (DI3325), Pathologies particulières (DI3370), Métabolisme (DI3223), Lipides, steroides, membranes (DI311C)
  • Unités de recherche UMONS : Biologie moléculaire (M122)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)
  • Centres UMONS : Mind & Health (CREMH)
Texte intégral :

Abstract(s) :

(Anglais) BACKGROUND: Central obesity is related to caloric excess promoting deleterious cellular responses in targeted organs. Nitric oxide (NO) has been determined as a key player in the pathogenesis of metabolic diseases. Here, we investigated the implication of inducible NO synthase (iNOS) in the development of obesity-induced kidney disease. MATERIALS AND METHODS: C57Bl/6 male mice were randomized to a low-fat diet (LFD) or a high-fat diet (HFD) and treated with L-NIL, a specific iNOS inhibitor for 16 weeks. RESULTS: Mice fed a HFD exhibited a significant increase in body weight, fasting blood glucose, plasma levels of NEFA, triglyceride and insulin. iNOS inhibition prevented these changes in mice fed a HFD. Interestingly, the significant increase in albuminuria and mesangial matrix expansion were not ameliorated with L-NIL whereas a significant decrease in proteinuria, NAG (N-acetyl-ß-D-glucosaminidase) excretion and renal triglycerides content were found, suggesting that iNOS inhibition is more suitable for tubular function than glomerular function. The urinary hydrogen peroxide level, a stable product of ROS production, that was found to be increased in mice fed a HFD, was significantly reduced with L-NIL. Finally, despite a moderate effect of L-NIL on inflammatory process in the kidney, we demonstrated a positive impact of this treatment on adipocyte hypertrophy and on adipose tissue inflammation. CONCLUSIONS: These results suggest that inhibition of iNOS leads to a moderate beneficial effect on kidney function in mice fed a HFD. Further studies are needed for better understanding of the role of iNOS in obesity-induced kidney disease. This article is protected by copyright. All rights reserved.