Advanced search
Start date
Betweenand
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

Full text
Author(s):
Aissa, Alexandre Ferro [1] ; Tryndyak, Volodymyr [2] ; de Conti, Aline [2] ; Melnyk, Stepan [3] ; Ursula Hermogenes Gomes, Tarsila Daysy [4] ; Pires Bianchi, Maria Lourdes [4] ; James, S. Jill [3] ; Beland, Frederick A. [2] ; Greggi Antunes, Lusania Maria [1, 4] ; Pogribny, Igor P. [2]
Total Authors: 10
Affiliation:
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Genet, Sao Paulo - Brazil
[2] US FDA, Div Biochem Toxicol, NCTR, Jefferson, AR 72079 - USA
[3] Univ Arkansas Med Sci, Dept Pediat, Little Rock, AR 72205 - USA
[4] Univ Sao Paulo, Fac Pharmaceut Sci Ribeirao Preto, Dept Clin Anal Toxicol & Food Sci, Sao Paulo - Brazil
Total Affiliations: 4
Document type: Journal article
Source: MOLECULAR NUTRITION & FOOD RESEARCH; v. 58, n. 7, p. 1502-1512, JUL 2014.
Web of Science Citations: 15
Abstract

Scope: A compromised nutritional status in methyl-group donors may provoke several molecular alterations triggering the development of nonalcoholic fatty liver disease (NAFLD) in humans and experimental animals. In this study, we investigated a role and the underlying molecular mechanisms of methionine metabolic pathway malfunctions in the pathogenesis of NAFLD. Methods and results: We fed female Swiss albino mice a control (methionine-adequate) diet and two experimental (methionine-deficient or methionine-supplemented) diets for 10 weeks, and the levels of one-carbon metabolites, expression of one-carbon and lipid metabolism genes in the livers were evaluated. We demonstrate that both experimental diets increased hepatic levels of S-adenosyl-L-homocysteine and homocysteine, altered expression of one-carbon and lipid metabolism genes, and caused lipid accumulation, especially in mice fed the methionine-deficient diet. Markers of oxidative and ER stress response were also elevated in the livers of mice fed either diet. Conclusion: Our findings indicate that both dietary methionine deficiency and methionine supplementation can induce molecular abnormalities in the liver associated with the development of NAFLD, including deregulation in lipid and one-carbon metabolic pathways, and induction of oxidative and ER stress. These pathophysiological events may ultimately lead to lipid accumulation in the livers, triggering the development of NAFLD. (AU)

FAPESP's process: 10/01410-0 - Gene-diet interaction in mice supplemented with methionine in the fetal and postnatal periods: studies of genomic instability, methylation and expression of genes related to cardiovascular diseases
Grantee:Alexandre Ferro Aissa
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 12/10872-2 - MicroRNA expression analysis in female mice treated with methionine-deficient or -supplemented diets during pregnancy
Grantee:Alexandre Ferro Aissa
Support type: Scholarships abroad - Research Internship - Doctorate