Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice.

Details

Serval ID
serval:BIB_7AF7A55FF7A8
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice.
Journal
Scientific reports
Author(s)
Yzydorczyk C., Li N., Chehade H., Mosig D., Bidho M., Keshavjee B., Armengaud J.B., Nardou K., Siddeek B., Benahmed M., Vergely C., Simeoni U.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Publication state
Published
Issued date
10/10/2017
Peer-reviewed
Oui
Volume
7
Number
1
Pages
12911
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Abstract
Unbalanced nutrition early in life is increasingly recognized as an important factor in the development of chronic, non-communicable diseases at adulthood, including metabolic diseases. We aimed to determine whether transient postnatal overfeeding (OF) leads to liver stress-induced premature senescence (SIPS) of hepatocytes in association with liver structure and hepatic function alterations. Litters sizes of male C57BL/6 mice were adjusted to 9 pups (normal feeding, NF) or reduced to 3 pups during the lactation period to induce transient postnatal OF. Compared to the NF group, seven-month-old adult mice transiently overfed during the postnatal period were overweight and developed glucose intolerance and insulin resistance. Their livers showed microsteatosis and fibrosis, while hepatic insulin signaling and glucose transporter protein expressions were altered. Increased hepatic oxidative stress (OS) was observed, with increased superoxide anion production, glucose-6-phosphate dehydrogenase protein expression, oxidative DNA damage and decreased levels of antioxidant defense markers, such as superoxide dismutase and catalase proteins. Hepatocyte senescence was characterized by increased p21 <sup>WAF</sup> , p53, Acp53, p16 <sup>INK4a</sup> and decreased pRb/Rb and Sirtuin-1 (SIRT-1) protein expression levels. Transient postnatal OF induces liver OS at adulthood, associated with hepatocyte SIPS and alterations in liver structure and hepatic functions, which could be mediated by a SIRT-1 deficiency.
Keywords
Aging/pathology, Animals, Animals, Newborn, Body Composition, Body Weight, DNA Damage, Female, Glucose/metabolism, Glucose Tolerance Test, Insulin/metabolism, Liver/metabolism, Liver/pathology, Liver Cirrhosis/pathology, Membrane Transport Proteins/metabolism, Mice, Inbred C57BL, Overnutrition/pathology, Oxidative Stress, Signal Transduction, Staining and Labeling, Stress, Physiological
Pubmed
Web of science
Open Access
Yes
Create date
19/10/2017 8:32
Last modification date
20/08/2019 15:36
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