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Dietary green tea extract (GT) lowers the plasma and hepatic triglyceride (TG) with an increase in plasma HDL‐cholesterol (HDL‐C) and decreases in SREBP1c mRNA and its responsive genes in fructose‐fed ovariectomized (OX) rats
Author(s) -
Shrestha Sudeep,
Ehlers Sarah J,
Lee JiYoung,
Fernandez Maria Luz,
Koo Sung I.
Publication year - 2007
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.21.5.a342-b
Subject(s) - medicine , endocrinology , fructose , triglyceride , fatty acid synthase , cholesterol , chemistry , lipid metabolism , biology , biochemistry
This study was conducted to determine the effect of GT on lipid metabolism in fructose‐fed OX rats. OX rats were assigned to the following groups with 7 each: a starch (S) group fed the AIN‐93G diet with corn starch as the major carbohydrate source a fructose (F) group fed the same diet but with 60% F; a group fed the F diet containing 0.5% GT; and another group fed the F diet containing 1% GT. At 6 wk, plasma and liver TG and cholesterol (CH), and HDL‐C, and expression of liver SREBP1c and related genes were determined. Fructose feeding significantly elevated plasma TG and TC compared with the S control. GT at 0.5 and 1.0% markedly lowered plasma TG and liver TG and CH. GT at 1.0% increased plasma CH with an increase in HDL‐C, compared with the F control. Fructose feeding significantly increased the abundance of liver SREBP1c, fatty acid synthase (FAS), and stearoyl‐CoA desaturase (SCD1) mRNAs compared with the S control, whereas GT decreased SREBP1c and FAS mRNAs and tended to decrease SCD1 mRNA. GT at 0.5% significantly decreased HMG‐CoA reductase mRNA compared with the F control. GT did not alter the expression of intestinal NPC1L1, SR‐B1, and ABCA1. The results, coupled with our earlier findings, suggest that the TG‐lowering effect of GT is mediated partly via its inhibition of intestinal absorption and liver synthesis of lipids involving SREBP1 and its responsive genes. Supported by NIH NCCAM Grant R21AT001363‐01A2 to SIK.