Renal mineralocorticoid receptor expression is reduced in lipoatrophy.

Détails

Ressource 1Télécharger: 30761257.pdf (551.33 [Ko])
Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_CC2FAFFB0EBF
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Renal mineralocorticoid receptor expression is reduced in lipoatrophy.
Périodique
FEBS open bio
Auteur(s)
Toffoli B., Bernardi S., Winkler C., Carrascosa C., Gilardi F., Desvergne B.
ISSN
2211-5463 (Print)
ISSN-L
2211-5463
Statut éditorial
Publié
Date de publication
02/2019
Peer-reviewed
Oui
Volume
9
Numéro
2
Pages
328-334
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
Obesity is a condition characterized by adipose tissue hypertrophy; it is estimated that the obesity epidemic accounted for 4 million deaths in 2015 and that 70% of these were due to cardiovascular disease (CVD). One of the mechanisms linking obesity to CVD is the ability of adipose tissue to secrete circulating factors. We hypothesized that adipose tissue and its secretory products may influence mineralocorticoid receptor (MR) expression. Here, we showed that expression of MR and its downstream targets (Cnksr3, Scnn1b, and Sgk1) were significantly reduced in the kidneys of peroxisome proliferator-activated receptor-γ null (Pparg <sup>
Δ/Δ
</sup> ) and A-ZIP/F-1 (AZIP <sup>tg/+</sup> ) lipoatrophic mice with respect to their controls. Intriguingly, MR expression was also found to be significantly reduced in the kidneys of genetically obese ob/ob mice. Our data suggest that adipose tissue contributes to the regulation of MR expression. Given that leptin deficiency seems to be the major feature shared by Pparg <sup>
Δ/Δ
</sup> , AZIP <sup>tg/+</sup> , and ob/ob mice, we speculate that adipose tissue modulates MR expression through the leptin system.
Mots-clé
kidney, lipoatrophy, mineralocorticoid receptor, obesity
Pubmed
Web of science
Open Access
Oui
Création de la notice
18/03/2019 17:32
Dernière modification de la notice
20/08/2019 15:46
Données d'usage