title: Possible molecular mechanisms soy-mediated in preventing and treating nonalcoholic fatty liver disease.
abstract: The aim of this review is to describe the molecular mechanisms of nonalcoholic fatty liver disease (NAFLD) and to present evidence regarding the mechanisms of soy-mediated therapeutic activity in preventing and treating NAFLD. NAFLD is induced by multiple metabolic pathways, including an increase in the release of fatty acids from the adipose tissue (lipolysis), insulin resistance (IR), and an increase in "de novo" fatty acid synthesis. Furthermore, NAFLD is correlated with a decrease in liver β-oxidation, an increase in oxygen free radical production, and an increase in pro-inflammatory cytokine production, which leads to an increase in liver fat and, subsequently, to tissue damage. The bioactive compounds in soy can prevent and treat NAFLD by modulating lipid metabolism and regulating the expression of related transcription factors. Soy intake decreases the expression of sterol regulatory-element binding protein-lc (SREBP-1) and increases the expression of SREBP-2, which are transcription factors associated with the regulation of hepatic lipogenesis and reduction of cholesterol synthesis and absorption in the liver, respectively. Besides, interactions between soy components, such as standard amino acids, polyunsaturated fat, and the isoflavonoid-enriched fraction, are believed to improve fatty acid oxidation in the liver parenchyma by increasing the expression of peroxisome proliferator-activated receptor α (PPARα)-regulated genes, thus decreasing lipid accumulation in the liver. Therefore, including soy-derived foods in the diet as a therapeutic tool for patients with NAFLD might improve their clinical evolution.
authors.affiliation: Nutrition Science Department, Bahía Federal University, Salvador, Bahia, Brazil. lucipmo@ufba.br
authors.forename: L P M
authors.initials: LP
authors.lastname: Oliveira
authors.forename: R P
authors.initials: RP
authors.lastname: de Jesús
authors.forename: T O
authors.initials: TO
authors.lastname: Freire
authors.forename: C P
authors.initials: CP
authors.lastname: Oliveira
authors.forename: A
authors.initials: A
authors.lastname: Castro Lyra
authors.forename: L G C
authors.initials: LG
authors.lastname: Lyra
mesh_terms: D000818:Animals; D004032:Diet; D005234:Fatty Liver / Q000517:prevention & control*; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects / Q000502:physiology; D065626:Non-alcoholic Fatty Liver Disease; D047493:PPAR alpha / Q000378:metabolism; D013025:Glycine max; D051780:Sterol Regulatory Element Binding Protein 1 / Q000378:metabolism; D051782:Sterol Regulatory Element Binding Protein 2 / Q000378:metabolism
chemical_list: D047493:PPAR alpha; C497387:SREBF1 protein, human; C497390:SREBF2 protein, human; D051780:Sterol Regulatory Element Binding Protein 1; D051782:Sterol Regulatory Element Binding Protein 2