Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways
BackgroundEarly 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...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2020-05-01
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| Series: | Frontiers in Physiology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fphys.2020.00511/full |
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| author | Christian Juvet Christian Juvet Benazir Siddeek Catherine Yzydorczyk Catherine Vergely Katya Nardou Jean-Baptiste Armengaud Jean-Baptiste Armengaud Mohamed Benahmed Umberto Simeoni Umberto Simeoni François Cachat Hassib Chehade Hassib Chehade |
| author_facet | Christian Juvet Christian Juvet Benazir Siddeek Catherine Yzydorczyk Catherine Vergely Katya Nardou Jean-Baptiste Armengaud Jean-Baptiste Armengaud Mohamed Benahmed Umberto Simeoni Umberto Simeoni François Cachat Hassib Chehade Hassib Chehade |
| author_sort | Christian Juvet |
| collection | DOAJ |
| description | BackgroundEarly 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.Materials and MethodsReduced 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.ResultsEarly 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.ConclusionEarly 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. |
| first_indexed | 2024-12-14T05:29:14Z |
| format | Article |
| id | doaj.art-52bd5ece8d094a84ab818bd0b6dc268b |
| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-12-14T05:29:14Z |
| publishDate | 2020-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Physiology |
| spelling | doaj.art-52bd5ece8d094a84ab818bd0b6dc268b2022-12-21T23:15:24ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2020-05-011110.3389/fphys.2020.00511518311Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence PathwaysChristian Juvet0Christian Juvet1Benazir Siddeek2Catherine Yzydorczyk3Catherine Vergely4Katya Nardou5Jean-Baptiste Armengaud6Jean-Baptiste Armengaud7Mohamed Benahmed8Umberto Simeoni9Umberto Simeoni10François Cachat11Hassib Chehade12Hassib Chehade13Division of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Woman-Mother-Child Department, Centre Hospitalier, Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandInserm UMR866, Laboratoire de Physiopathologie et Pharmacologie Cardio-Métaboliques (LPPCM), Faculties of Medicine and Pharmacy, University of Burgundy, Dijon, FranceDivision of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Woman-Mother-Child Department, Centre Hospitalier, Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Woman-Mother-Child Department, Centre Hospitalier, Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Pediatric Nephrology Unit, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Developmental Origins of Health and Disease (DOHaD) Laboratory, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandDivision of Pediatrics, Pediatric Nephrology Unit, Woman-Mother-Child Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, SwitzerlandBackgroundEarly 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.Materials and MethodsReduced 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.ResultsEarly 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.ConclusionEarly 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.https://www.frontiersin.org/article/10.3389/fphys.2020.00511/fullprogrammingovernutritionpostnatal overfeedingkidneychronic kidney diseasedevelopmental origins of health and disease |
| spellingShingle | Christian Juvet Christian Juvet Benazir Siddeek Catherine Yzydorczyk Catherine Vergely Katya Nardou Jean-Baptiste Armengaud Jean-Baptiste Armengaud Mohamed Benahmed Umberto Simeoni Umberto Simeoni François Cachat Hassib Chehade Hassib Chehade Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways Frontiers in Physiology programming overnutrition postnatal overfeeding kidney chronic kidney disease developmental origins of health and disease |
| title | Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways |
| title_full | Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways |
| title_fullStr | Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways |
| title_full_unstemmed | Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways |
| title_short | Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways |
| title_sort | renal programming by transient postnatal overfeeding the role of senescence pathways |
| topic | programming overnutrition postnatal overfeeding kidney chronic kidney disease developmental origins of health and disease |
| url | https://www.frontiersin.org/article/10.3389/fphys.2020.00511/full |
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