DI-UMONS : Dépôt institutionnel de l’université de Mons

Recherche transversale
(titres de publication, de périodique et noms de colloque inclus)
2020-12-31 - Article/Dans un journal avec peer-review - Anglais - 20 page(s)

Juszczak Florian , Vlassembrouck Maud, Botton Olivia, Zwakhals Thomas , Decarnoncle Morgane , Tassin Alexandra , Caron Nathalie, Decleves Anne-Emilie , "Delayed Exercise Training Improves Obesity-Induced ChronicKidney Disease by Activating AMPK Pathway in High-FatDiet-Fed Mice" in International Journal of Molecular Sciences, 22, 1, 10.3390/ijms22010350

  • Edition : Multidisciplinary Digital Publishing Institute (MDPI) (Switzerland)
  • Codes CREF : Néphrologie - urologie (DI3325), Biologie moléculaire (DI3111), Pathologies particulières (DI3370)
  • Unités de recherche UMONS : Biochimie métabolique et moléculaire (M122)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)
  • Centres UMONS : Mind & Health (CREMH)
Texte intégral :

Abstract(s) :

(Anglais) Exercise training is now recognized as an interesting therapeutic strategy in managing obesity and its related disorders. However, there is still a lack of knowledge about its impact on obesity-induced chronic kidney disease (CKD). Here, we investigated the effects of a delayed protocol of endurance exercise training (EET) as well as the underlying mechanism in obese mice presenting CKD. Mice fed a high-fat diet (HFD) or a low-fat diet (LFD) for 12 weeks were subsequently submitted to an 8-weeks EET protocol. Delayed treatment with EET in obese mice prevented body weight gain associated with a reduced calorie intake. EET intervention counteracted obesity-related disorders including glucose intolerance, insulin resistance, dyslipidaemia and hepatic steatosis. Moreover, our data demonstrated for the first time the beneficial effects of EET on obesity-induced CKD as evidenced by an improvement of obesity-related glomerulopathy, tubulo-interstitial fibrosis, inflammation and oxidative stress. EET also prevented renal lipid depositions in the proximal tubule. These results were associated with an improvement of the AMPK pathway by EET in renal tissue. AMPK-mediated phosphorylation of ACC and ULK-1 were particularly enhanced leading to increased fatty acid oxidation and autophagy improvement with EET in obese mice.

Identifiants :
  • DOI : 10.3390/ijms22010350

Mots-clés :
  • (Anglais) chronic kidney disease
  • (Anglais) endurance exercise training
  • (Anglais) AMPK
  • (Anglais) high-fat diet
  • (Anglais) ectopic lipid accumulation
  • (Anglais) autophagy