Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-10-10

AUTHORS

Catherine Yzydorczyk, Na Li, Hassib Chehade, Dolores Mosig, Mickael Bidho, Basile Keshavjee, Jean Baptiste Armengaud, Katya Nardou, Benazir Siddeek, Mohamed Benahmed, Catherine Vergely, Umberto Simeoni

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 p21WAF, p53, Acp53, p16INK4a 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. More... »

PAGES

12911

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-017-11756-2

DOI

http://dx.doi.org/10.1038/s41598-017-11756-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1092092317

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29018245


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35 schema:description 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.
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43 C57BL/6 mice
44 DNA damage
45 NF group
46 Rb
47 SIRT-1 deficiency
48 Sirtuin-1 (SIRT-1) protein expression levels
49 adult mice
50 adulthood
51 alterations
52 anion production
53 antioxidant defense markers
54 association
55 catalase protein
56 chronic
57 damage
58 defense markers
59 deficiency
60 dehydrogenase protein expression
61 development
62 development of chronic
63 disease
64 dismutase
65 expression
66 expression levels
67 factors
68 fibrosis
69 function
70 function alterations
71 glucose intolerance
72 glucose transporter protein expression
73 glucose-6-phosphate dehydrogenase protein expression
74 group
75 hepatic function
76 hepatic function alterations
77 hepatic insulin
78 hepatic oxidative stress
79 hepatocyte SIPS
80 hepatocyte senescence
81 hepatocytes
82 important factor
83 induces liver OS
84 insulin
85 insulin resistance
86 intolerance
87 lactation period
88 levels
89 life
90 litter size
91 liver
92 liver OS
93 liver stress-induced premature senescence
94 liver structure
95 male C57BL/6 mice
96 markers
97 metabolic diseases
98 mice
99 microsteatosis
100 non-communicable diseases
101 nutrition
102 overfeeding
103 oxidative DNA damage
104 oxidative stress
105 p16
106 p21
107 p53
108 period
109 postnatal
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111 postnatal period
112 premature senescence
113 production
114 protein
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117 pups
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120 seven-month-old adult mice
121 size
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124 structure
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127 superoxide dismutase
128 transient postnatal
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130 transporter protein expression
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