Author:
Benoit Berengère,Beau Alice,Bres Émilie,Chanon Stéphanie,Pinteur Claudie,Vieille-Marchiset Aurélie,Jalabert Audrey,Zhang Hao,Garg Priyanka,Strigini Maura,Vico Laurence,Ruzzin Jérôme,Vidal Hubert,Koppe Laetitia
Abstract
AbstractChronic kidney disease (CKD) is associated with osteosarcopenia, and because a physical decline in patients correlates with an increased risk of morbidity, an improvement of the musculoskeletal system is expected to improve morbi-mortality. We recently uncovered that the intestinal hormone Fibroblast Growth Factor 19 (FGF19) is able to promote skeletal muscle mass and strength in rodent models, in addition to its capacity to improve glucose homeostasis. Here, we tested the effects of a treatment with recombinant human FGF19 in a CKD mouse model, which associates sarcopenia and metabolic disorders. In 5/6 nephrectomized (5/6Nx) mice, subcutaneous FGF19 injection (0.1 mg/kg) during 18 days increased skeletal muscle fiber size independently of food intake and weight gain, associated with decreased gene expression of myostatin. Furthermore, FGF19 treatment attenuated glucose intolerance and reduced hepatic expression of gluconeogenic genes in uremic mice. Importantly, the treatment also decreased gene expression of liver inflammatory markers in CKD mice. Therefore, our results suggest that FGF19 may represent a novel interesting therapeutic strategy for a global improvement of sarcopenia and metabolic complications in CKD.
Funder
BONTON-19
Société Francophone de Néphrologie Dialyse Transplantation
MS by Fonds d’amorçage Recherche de la Fondation UJM.
ARMOE (Aide à la Recherche Médicale Ondaine et Environs)
Publisher
Springer Science and Business Media LLC
Cited by
4 articles.
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