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Expression profiling of hepatic genes associated with lipid metabolism in nephrotic rats
Author(s) -
Guan Youfei,
Zhou Yunfeng,
Zhang Xiaoyan,
Chen Lihong,
Wei Mingfen,
Zhang Yahua
Publication year - 2008
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.22.1_supplement.948.7
Subject(s) - lipid metabolism , fatty acid metabolism , hypertriglyceridemia , fatty acid synthesis , metabolism , biology , fatty acid , gene , beta oxidation , triglyceride , endocrinology , biosynthesis , medicine , biochemistry , cholesterol
Hyperlipidemia is one of the major features of nephrotic syndrome (NS) and the underlying mechanisms remain largely uncharacterized. The present study was designed to examine the gene profile associated with lipid metabolism in the livers of nephrotic rats. NS was made in male rats (n=6) receiving sequential i.p injections of puromycin aminonucleoside. An Affymetrix assay, the quantitative PCR, and immunoblot identified 12 genes associated with cholesterol metabolism and 9 genes associated with fatty acid metabolism. Eight genes involved in cholesterol metabolism including Apo A‐I, Acly, Acat, Mpd, Fdps, Ss, Lss, and Nsdhl were significantly upregulated. Four genes involved in fatty acid biosynthesis including Acc, FAS, ELOVL 2 and 6 and three genes critical for triglyceride biosynthesis including Gpam, Agpat 3 and Dgat 1 were significantly induced, while two genes involved in fatty acid oxidation including Dci and MCAD were downregulated. Expression of several genes leading to SREBP‐1 activation was also altered. Collectively, induction of genes involved in cholesterol biosynthesis may be responsible for hypercholesterolemia, while upregulation of genes participated in fatty acid and triglyceride biosynthesis, and reduction of genes involved in fatty acid oxidation may contribute to hypertriglyceridemia in nephrotic rats. Overactivation of SREBP‐1 pathway may represent an underlying mechanism.