title: Dietary soya protein concentrate enriched with isoflavones reduced fatty liver, increased hepatic fatty acid oxidation and decreased the hepatic mRNA level of VLDL receptor in obese Zucker rats.
abstract: Casein-based diets containing a low (LDI) or high (HDI) dose of soya protein concentrate enriched with isoflavones were fed to obese Zucker rats for 6 weeks. HDI feeding, but not LDI feeding, reduced the fatty liver and decreased the plasma levels of alanine transaminase and aspartate transaminase. This was accompanied by increased activities of mitochondrial and peroxisomal beta-oxidation, acetyl-CoA carboxylase, fatty acid synthase and glycerol-3-phosphate acyltransferase in liver and increased triacylglycerol level in plasma. The decreased fatty liver and the increased plasma triacylglycerol level appeared not to be caused by an increased secretion of VLDL, as HDI decreased the hepatic mRNA levels of apo B and arylacetamide deacetylase. However, the gene expression of VLDL receptor was markedly decreased in liver, but unchanged in epididymal white adipose tissue and skeletal muscle of rats fed HDI, indicating that the liver may be the key organ for the reduced clearance of triacylglycerol-rich lipoproteins from plasma after HDI feeding. The n-3/n-6, 20:4n-6/18:2n-6 and (20:5n-3+22:6n-3)/18:3n-3 ratios were increased in liver triacylglycerol by HDI. The phospholipids in liver of rats fed HDI contained a low level of 20:4n-6 and a high level of 20:5n-3, favouring the production of anti-inflammatory eicosanoids. When obese Zucker rats were fed soya protein, this also resulted in reduced fatty liver, possibly through reduced clearance of VLDL by the liver. We conclude that the isoflavone-enriched soya concentrate as well as soya protein may be promising dietary supplements for treatment of non-alcoholic fatty liver.
authors.affiliation: Institute of Medicine, Section of Medical Biochemistry, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway. nkjgu@uib.no
authors.forename: Oddrun A
authors.initials: OA
authors.lastname: Gudbrandsen
authors.forename: Hege
authors.initials: H
authors.lastname: Wergedahl
authors.forename: Sverre
authors.initials: S
authors.lastname: Mørk
authors.forename: Bjørn
authors.initials: B
authors.lastname: Liaset
authors.forename: Marit
authors.initials: M
authors.lastname: Espe
authors.forename: Rolf K
authors.initials: RK
authors.lastname: Berge
mesh_terms: D000818:Animals; D019587:Dietary Supplements; D005227:Fatty Acids / Q000378:metabolism; D005234:Fatty Liver / Q000178:diet therapy* / Q000209:etiology / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D007529:Isoflavones / Q000627:therapeutic use*; D050356:Lipid Metabolism / Q000187:drug effects; D008099:Liver / Q000378:metabolism*; D008297:Male; D009765:Obesity / Q000150:complications / Q000378:metabolism; D010084:Oxidation-Reduction; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011924:Rats, Zucker; D011973:Receptors, LDL / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D030262:Soybean Proteins / Q000627:therapeutic use*
chemical_list: D005227:Fatty Acids; D007529:Isoflavones; D012333:RNA, Messenger; D011973:Receptors, LDL; D030262:Soybean Proteins; C036053:VLDL receptor