Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways.

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Version: Final published version
License: CC BY 4.0
Serval ID
serval:BIB_CD0020442960
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways.
Journal
Frontiers in physiology
Author(s)
Juvet C., Siddeek B., Yzydorczyk C., Vergely C., Nardou K., Armengaud J.B., Benahmed M., Simeoni U., Cachat F., Chehade H.
ISSN
1664-042X (Print)
ISSN-L
1664-042X
Publication state
Published
Issued date
2020
Peer-reviewed
Oui
Volume
11
Pages
511
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Early nutrition influences the risk of chronic kidney diseases (CKDs) development in adulthood. Mechanisms underlying the early programming of altered renal function remain incompletely understood. This study aims at characterizing the role of cell senescence pathways in early programming of CKD after transient postnatal overfeeding.
Reduced litters of 3 mice pups and standard litters of 9 mice pups were obtained to induce overfed animals during lactation and control animals, respectively. Animals were sacrificed at 24 days (weaning) or at 7 months of life (adulthood). Body weight, blood pressure, kidney weight, and glomerular count were assessed in both groups. Senescence pathways were investigated using β-Galactosidase staining and Western blotting of P16, P21, P53, P-Rb/Rb, and Sirtuin 1 (Sirt1) proteins.
Early overfed animals had a higher body weight, a higher blood pressure at adulthood, and a higher glomerular number endowment compared to the control group. A higher β-Galactosidase activity, a significant increase in P53 protein expression (p = 0.0045) and a significant decrease in P-Rb/Rb ratio (p = 0.02), were observed at weaning in animals who underwent early postnatal overfeeding. Protein expression of Sirt1, a protective factor against accelerated stress-induced senescence, was significantly decreased (p = 0.03) at weaning in early overfed animals.
Early postnatal overfeeding by litter size reduction is associated with increased expression of factors involved in cellular senescence pathways, and decreased expression of Sirt 1 in the mouse kidney at weaning. These alterations may contribute to CKD programming after early postnatal overfeeding.
Keywords
chronic kidney disease, developmental origins of health and disease, kidney, overnutrition, postnatal overfeeding, programming
Pubmed
Web of science
Open Access
Yes
Create date
25/06/2020 15:52
Last modification date
15/01/2021 7:11
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