Aldr KO mice in liver with Fenofibrate treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Agatha Schluter
PROVIDER: E-MTAB-2006 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Fenofibrate is a specific agonist of the nuclear receptor PPARa. To identify the gene expression under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice. We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice. There are 36 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 14 week-old from the same genetic background (C57Bl/6J) treated with Fenofibrate (100 mg/kg/day) or vehicle (aqueous solution of gum Arabic 3%) by daily gavage for 10 days. n= 4 mice for LKO, LWT and WT genotypes treated with vehicle; n=3 for KO mice treated with vehicle; n=5 mice for LWT, LKO and KO genotypes treated with fenofibrate; n=4 WT mice treated with fenofibrate. All mice were sacrified at ZT14.
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Project description:Elevated circulating triglycerides, which are considered a risk factor for cardiovascular disease, can be targeted by treatment with fenofibrate or fish oil. To gain insight into underlying mechanisms, we carried out a comparative transcriptomics and metabolomics analysis of the effect of 2 week treatment withfenofibrate and fish oil in mice. Plasma triglycerides were significantly decreased byfenofibrate (-49.1%) and fish oil (-21.8%), whereas plasma cholesterol was increased by fenofibrate (+29.9%) and decreased by fish oil (-32.8%). Levels of various phospholipid species were specifically decreased by fish oil, while levels of Krebs cycle intermediates were increased specifically by fenofibrate. Plasma levels of many amino acids were altered by fenofibrate and to a lesser extent by fish oil. Both fenofibrate and fish oil upregulated genes involved in fatty acid metabolism, and downregulated genes involved in blood coagulation and fibrinolysis. Significant overlap in gene regulation by fenofibrate and fish oil was observed, reflecting their property as high or low affinity agonist for PPARα, respectively. Fenofibrate specifically downregulated genes involved in complement cascade and inflammatory response. Fish oil specifically downregulated genes involved in cholesterol and fatty acid biosynthesis, and upregulated genes involved in amino acid and arachidonic acid metabolism. Taken together, the data indicate that despite being similarly potent towards modulating plasma free fatty acids, cholesterol and triglyceride levels, fish oil causes modest changes in gene expression likely via activation of multiple mechanistic pathways, whereas fenofibrate causes pronounced gene expression changes via a single pathway, reflecting the key difference between nutritional and pharmacological intervention. Expression profiling of liver from mice fed control diet, fish oil or fenofibrate for 2 weeks.
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Project description:C57BL/6 mice were fed ad libitum for the first 5 days of the experiments with high fat high cholesterol (HFC) diet only. The next 7 days of the experiments mice were continuously fed on a HFC diet and simultaneously vehicle (control group), fenofibrate (100 mg/kg) or lovastatin (30 mg/kg) were orally daily administered. At the end of the experiment (day 12) fenofibrate and lovastatin significantly decreased plasma LDL levels, while plasma cholesterol levels were significantly decreased by lovastatin only. Gene expression analysis of hyperlipidemic mouse liver revealed 391 significantly modulated genes when compared to standard diet fed mice. KEGG pathways related to modulated genes were identified and the most significant were biosynthesis of steroids, metabolism of xenobiotics by cytochrome P450 and linoleic acid metabolism. These pathways were modulated in a way, which increased the clearance of lipids and decreased endogenous synthesis of fatty acids and cholesterol. Additionally, genes involved in the regulation of detoxification pathways were significantly upregulated. The hepatic gene expression profiles of fenofibrate and lovastatin-treated HFC diet fed mice were compared to the vehicle-treated HFC diet fed mice. In the fenofibrate-treated group 124 genes and in the lovastatin-treated group 38 genes were significantly modulated. In the fenofibrate-treated group the top three significantly modulated pathways are fatty acid metabolism, propanoate metabolism and ascorbate and aldarate metabolism. While in the lovastatin-treated group the top three significantly modulated pathways are glycosphingolipid biosynthesis, tyrosine metabolism and metabolism of xenobiotics by cytochrome P450. Expert based classification revealed that both fenofibrate an lovastatin significantly down-regulated genes encoding sterol-C4-methyl oxidase like and 7-dehydrocholesterol reductase. Additionally, the regulation of cholesterol at the transcriptional level was also significantly augmented by fenofibrate and lovastatin, as judged by increased expression of -1 and decreased expression of INSIG-2. Experiment Overall Design: 24 seven week old mice were randomly divided in four experimental groups. Control group (n = 6) was fed on a standard chow diet (diet 3430, Provimi Kliba AG, Kaiseraugst, Switzerland) and treated orally once daily with vehicle for 12 days. Remaining 18 mice were fed on HFC diet for 12 days. On day five HFC diet fed mice were treated orally once daily either with vehicle (HFC group, n=6), lovastatin (HFC lovastatin group, 30mg/kg, n=6) or fenofibrate (HFC fenofibrate group, 100mg/kg, n=6). Doses of lovastatin and fenofibrate were choosen according to the literature review. On day 12 liver were excised and immediately frozen in liquid nitrogen and stored at -80°C for the subsequent transriptome analyses
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