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Soy Protein regulates differently reverse cholesterol transport in liver and ileum in mice.
Author(s) -
Granados Omar,
GonzalezGranillo Marcela,
Torres Nimbe,
Tovar Armando R
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.937.5
Subject(s) - abca1 , liver x receptor , medicine , endocrinology , cholesterol , bile acid , reverse cholesterol transport , ileum , steatosis , excretion , biology , liver x receptor alpha , chemistry , transporter , biochemistry , lipoprotein , nuclear receptor , transcription factor , gene
Liver X alpha‐receptor (LXRα) is activated by oxysterols that regulates ABCG5, ABCG8 and ABCA1 gene expression involved in the reverse cholesterol transport (RCT). Up‐regulation increases biliary cholesterol secretion and limits cholesterol (CH) absorption. Studies in rats have demonstrated that soy protein (SP) has hypocholesterolemic effect through an increase in bile acid secretion. In the present study, we evaluated the effect of a high CH SP or casein diet on the expression of ABCG5, ABCG8, ABCA1 transporters in ileum and liver of wild‐type and LXRα knockout mice. We demonstrated that the absence of hepatic LXRα increased hepatic lipid concentration particularly with the high CH diets. Liver of mice fed with SP showed less macro‐vesicular steatosis, lipid accumulation and inflammatory infiltration independently of genotype and presence of CH in the diet. The absence of LXRα greatly reduced hepatic ABCG5, ABCG8 and ABCA1 mRNA expression with respect to the amount of hepatic CH concentration. However, the expression of these transporters in ileum of wild‐type group was higher in the SP+CH group than the group fed casein+CH. In addition, animals fed with SP+CH showed a higher excretion of fecal bile acids compared to casein+CH group. These results indicates that SP increases bile acid excretion through an increase in the ABC transporters despite the lack of LXRα. Supported by CONACYT Grant No 84786 (to O.G)
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