Unknown,Transcriptomics,Genomics,Proteomics

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Persistent Organic Pollutants cause insulin resistance and ruin the health effects of salmon oil

ABSTRACT: Transcriptional profiling of Rat liver submitted to high fat diets made with either crude (HFC) or refined salmon oil (HFR). Keywords: transcriptomic analysis Two groups of rats were submitted to high fat diet containing either crude salmon oil (HFC) or refined salmon oil (HFR). After 28 days, livers were retrieved and RNA extracted. A pool of RNA from HFR group was used as the reference group. Each HFC was compared to reference group (pool of HFR). Five biological replicates were processed.

ORGANISM(S): Rattus norvegicus

SUBMITTER: emmanuelle meugnier

PROVIDER: E-GEOD-13716 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Persistent organic pollutant exposure leads to insulin resistance syndrome.

Ruzzin Jérôme J Petersen Rasmus R Meugnier Emmanuelle E Madsen Lise L Lock Erik-Jan EJ Lillefosse Haldis H Ma Tao T Pesenti Sandra S Sonne Si Brask SB Marstrand Troels Torben TT Malde Marian Kjellevold MK Du Zhen-Yu ZY Chavey Carine C Fajas Lluis L Lundebye Anne-Katrine AK Brand Christian Lehn CL Vidal Hubert H Kristiansen Karsten K Frøyland Livar L

Environmental health perspectives 20091119 4

<h4>Background</h4>The incidence of the insulin resistance syndrome has increased at an alarming rate worldwide, creating a serious challenge to public health care in the 21st century. Recently, epidemiological studies have associated the prevalence of type 2 diabetes with elevated body burdens of persistent organic pollutants (POPs). However, experimental evidence demonstrating a causal link between POPs and the development of insulin resistance is lacking.<h4>Objective</h4>We investigated whet ...[more]

PMID: 20064776

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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 -80Â°C for the subsequent transriptome analyses

Dataset Information

Persistent Organic Pollutants cause insulin resistance and ruin the health effects of salmon oil

Publications

Persistent organic pollutant exposure leads to insulin resistance syndrome.

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