Effect of methionine‐deficient and methionine‐supplemented diets on the hepatic one‐carbon and lipid metabolism in mice

Aissa, Alexandre Ferro; Tryndyak, Volodymyr; Conti, Aline de; Melnyk, Stepan; Gomes, Tamara Maria; Bianchi, Marcelo; James, S. Jill; Beland, Frederick A.; Antunes, Lusânia Maria Greggi; Pogribny, Igor P.

doi:10.1002/mnfr.201300726

Cited by 45 publications

(36 citation statements)

References 53 publications

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“…In a subsequent study, using a panel of 7 genetically diverse inbred mouse strains (14), we demonstrated that the development of a strain-dependent NASH-like liver injury induced by a 12-wk dietary choline-and folate deficiency is paralleled by a prominent dysregulation in lipid and 1-carbon metabolism. Similar findings were reported in the livers of mice fed a methionine-deficient diet for 10 wk (15).…”

supporting

confidence: 87%

“…The development of NASH and NASH-related liver carcinogenesis has been associated with genetic, genomic, and metabolic abnormalities, with alterations in hepatic lipid homeostasis being one of the most prominent (11). In our studies, using a mouse model of NAFLD induced by a choline-and folate-deficient (CFD) (12)(13)(14) or methioninedeficient (15) diet, we found that the development of NASH is characterized by a profound and interconnected dysregulation in hepatic folate-dependent 1-carbon and lipid metabolism. Specifically, feeding C57BL/6J and DBA/2J mice a CFD diet for 18 wk resulted in an extensive hepatic lipid accumulation, prominent alterations in methyl donor metabolism, and development of NASH (12).…”

mentioning

confidence: 96%

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Epigenetically mediated inhibition of S‐adenosylhomocysteine hydrolase and the associated dysregulation of 1‐carbon metabolism in nonalcoholic steatohepatitis and hepatocellular carcinoma

et al. 2018

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The substantial rise in the prevalence of nonalcoholic steatohepatitis (NASH), an advanced form of nonalcoholic fatty liver disease, and the strong association between NASH and the development of hepatocellular carcinoma indicate the urgent need for a better understanding of the underlying mechanisms. In the present study, by using the Stelic animal model of NASH and NASH-derived liver carcinogenesis, we investigated the role of the folate-dependent 1-carbon metabolism in the pathogenesis of NASH. We demonstrated that advanced NASH and NASH-related liver carcinogenesis are characterized by a significant dysregulation of 1-carbon homeostasis, with diminished expression of key 1-carbon metabolism genes, especially a marked inhibition of the S-adenosylhomocysteine hydrolase ( Ahcy) gene and an increased level of S-adenosyl-l-homocysteine (SAH). The reduction in Ahcy expression was associated with gene-specific cytosine DNA hypermethylation and enrichment of the gene promoter by trimethylated histone H3 lysine 27 and deacetylated histone H4 lysine 16, 2 main transcription-inhibiting markers. These results indicate that epigenetically mediated inhibition of Ahcy expression may be a driving force in causing SAH elevation and subsequent downstream disturbances in transsulfuration and transmethylation pathways during the development and progression of NASH.-Pogribny, I. P., Dreval, K., Kindrat, I., Melnyk, S., Jimenez, L., de Conti, A., Tryndyak, V., Pogribna, M., Ortega, J. F., James, S. J., Rusyn, I., Beland, F. A. Epigenetically mediated inhibition of S-adenosylhomocysteine hydrolase and the associated dysregulation of 1-carbon metabolism in nonalcoholic steatohepatitis and hepatocellular carcinoma.

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supporting

confidence: 87%

mentioning

confidence: 96%

Epigenetically mediated inhibition of S‐adenosylhomocysteine hydrolase and the associated dysregulation of 1‐carbon metabolism in nonalcoholic steatohepatitis and hepatocellular carcinoma

et al. 2018

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“…The data are consistent with Aissa et al. () and Tapiarojas et al. () who reported that excessive Met supplementation induced oxidative stress, possibly due to that dietary Met supplementation increased the levels of fatty acid synthesis and oxidation (Skiba‐Cassy, Geurden, Panserat, & Seiliez, ).…”

Section: Discussionsupporting

confidence: 91%

A comparison of two sources of methionine supplemented at different levels on heat shock protein 70 expression and oxidative stress product of Peking ducks subjected to heat stress

Guo

Zhang

et al. 2017

Animal Physiology Nutrition

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SummaryThe aim of this study was to examine the effects of different sources and levels of | INTRODUCTIONBirds were vulnerable to high temperatures during summer because of the insufficient heat dissipation after a meal, especially possible for waterfowl (e.g., duck). Heat stress (HS) badly effects on both immune function and production (Humphrey, 2006). Further, HS results in negative effects on growth performance and the relevant mechanisms were explored to mitigate the negative effects (Quinteirofilho et al., 2010;Quinteiro-Filho et al., 2012;Sandhu, Mirza, Afzal, & Mukhtar, 2012;Song et al., 2013). On the cellular level, high temperature promotes proteolysis and induces the production of excessive free radicals which caused oxidative stress damaging different organs of the body (Del Vesco et al., 2015), such as the liver and intestine. | MATERIALS AND METHODSThe study was conducted in a research farm (Hebei, China), and all procedures described here were approved by the Institutional Animal Care and Use Committee of the China Agricultural University (Beijing, China). | Animals and dietsA total of 720 four-day-old Peking ducks were randomly allotted to Table 1. And, the highest, the lowest and the comfortable temperature during study are shown in Table 2. In addition, mortality was recorded daily during the entire trial. And, mortality was almost no. | Sample collectionSix birds per treatment were randomly selected at 16 and 35 day age and euthanized by CO 2 inhalation and decapitation. Liver samples (~2 g) were collected and separated into two portions. Tissue samples were snap frozen immediately in liquid nitrogen and then stored at −80°C and −40°C until further qRT-PCR and protein carbonylation content analyses respectively. Tissue samples (~5-8 mm) were taken

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“…In mice, modulation of dietary methionine can alter Srebf expression by feedback induction (Aissa et al, 2014). Similarly, expression of methionine metabolism genes in C. elegans not only depends on SREBF1 (SBP-1), but also feeds back to control SREBF1 and affect lipid metabolism (Walker et al, 2011).…”

Section: Ec Signaling Regulates Methionine Metabolism Via Srebfsmentioning

confidence: 99%

Cannabinoid receptor signaling regulates liver development and metabolism

et al. 2016

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Endocannabinoid (EC) signaling mediates psychotropic effects and regulates appetite. By contrast, potential roles in organ development and embryonic energy consumption remain unknown. Here, we demonstrate that genetic or chemical inhibition of cannabinoid receptor (Cnr) activity disrupts liver development and metabolic function in zebrafish (Danio rerio), impacting hepatic differentiation, but not endodermal specification: loss of cannabinoid receptor 1 (cnr1) and cnr2 activity leads to smaller livers with fewer hepatocytes, reduced liver-specific gene expression and proliferation. Functional assays reveal abnormal biliary anatomy and lipid handling. Adult cnr2 mutants are susceptible to hepatic steatosis. Metabolomic analysis reveals reduced methionine content in Cnr mutants. Methionine supplementation rescues developmental and metabolic defects in Cnr mutant livers, suggesting a causal relationship between EC signaling, methionine deficiency and impaired liver development. The effect of Cnr on methionine metabolism is regulated by sterol regulatory element-binding transcription factors (Srebfs), as their overexpression rescues Cnr mutant liver phenotypes in a methioninedependent manner. Our work describes a novel developmental role for EC signaling, whereby Cnr-mediated regulation of Srebfs and methionine metabolism impacts liver development and function.

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Effect of methionine‐deficient and methionine‐supplemented diets on the hepatic one‐carbon and lipid metabolism in mice

Cited by 45 publications

References 53 publications

Epigenetically mediated inhibition of S‐adenosylhomocysteine hydrolase and the associated dysregulation of 1‐carbon metabolism in nonalcoholic steatohepatitis and hepatocellular carcinoma

Epigenetically mediated inhibition of S‐adenosylhomocysteine hydrolase and the associated dysregulation of 1‐carbon metabolism in nonalcoholic steatohepatitis and hepatocellular carcinoma

A comparison of two sources of methionine supplemented at different levels on heat shock protein 70 expression and oxidative stress product of Peking ducks subjected to heat stress

Cannabinoid receptor signaling regulates liver development and metabolism

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