ArticleMolecular and cellular biochemistry2009
Effects of high dietary fat and cholesterol on expression of PPAR alpha, LXR alpha, and their responsive genes in the liver of apoE and LDLR double deficient mice.
Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Cornelian Cherry (International journal of molecular sciences · 2024Article
- Integrated lipidomic and transcriptomic analysis reveals clarithromycin-induced alteration of glycerophospholipid metabolism in the cerebral cortex of mice.Cell biology and toxicology · 2023Article
- Dietary cholesterol promotes growth and ecdysone signalling pathway by modulating cholesterol transport in swimming crabs (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2022Article
- Cornelian Cherry (Nutrients · 2021Article
- ANGPLT3 in cardio-metabolic disorders.Molecular biology reports · 2021Review
- Apolipoprotein F: a natural inhibitor of cholesteryl ester transfer protein and a key regulator of lipoprotein metabolism.Current opinion in lipidology · 2020Review
- Supplementation with an insoluble fiber obtained from carob pod (Ceratonia siliqua L.) rich in polyphenols prevents dyslipidemia in rabbits through SIRT1/PGC-1α pathway.European journal of nutrition · 2019Article
- Role of xenobiotics in the induction and progression of fatty liver disease.Toxicology research · 2018Review
- Triptolide inhibits the progression of atherosclerosis in apolipoprotein EExperimental and therapeutic medicine · 2016Article
- Lipid abnormalities in alpha/beta2-syntrophin null mice are independent from ABCA1.Biochimica et biophysica acta · 2015Article
- Western diet in ApoE-LDLR double-deficient mouse model of atherosclerosis leads to hepatic steatosis, fibrosis, and tumorigenesis.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- PPARα-dependent exacerbation of experimental colitis by the hypolipidemic drug fenofibrate.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Obesity and lipid stress inhibit carnitine acetyltransferase activity.Journal of lipid research · 2014Article
- ABCG5 gene responses to treadmill running with or without administration of Pistachio atlantica in female rats.Iranian journal of basic medical sciences · 2014Article
- Effects of a fixed-intensity of endurance training and pistacia atlantica supplementation on ATP-binding cassette G4 expression.Chinese medicine · 2013Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The significance of transcription factors PPAR alpha, LXR alpha, and their responsive/target genes for the pathogenesis of atherosclerosis in apolipoprotein E and low-density lipoprotein receptor double deficient (AL) mice fed with high fat and cholesterol (HF) diet were studied. C57BL/6J wild-type (WT) mice were used as control to the AL mice. Plasma lipid metabolites and morphological atherosclerotic lesions in aortic wall were determined. Semi- and real-time quantitative RT-PCR were used to measure gene expression patterns between AL mice and the controls, which were fed with HF or normal chow diet. The results showed that in AL mice fed with HF diet, plasma lipid levels, hepatic lipid accumulation, and atherogenesis together with upregulated PPAR alpha, LXR alpha, and their target genes, i.e., FAT, SCD1, FAS, Angptl3, and apoB100 significantly increased in a 12-week long feeding period. In contrast, apoAI, apoAIV, apoF, LPL, and SR-BI were decreased compared to chow-fed group. In WT mice, PPAR alpha, LXR alpha, FAS, Angpt13, CPT1, apoF, ACOX1, LPL, and SR-BI were increased with HF treatment, while apoAI and apoAIV were decreased markedly. The different changes of lipid metabolism-related genes between AL and WT mice, fed with HF diet or chow diet indicated that the mechanisms of dietary effects on gene mutant mice are different from those of intact WT mice. Since lipid metabolic system defected genetically in AL mice, we suggest that the changes of PPAR alpha, LXR alpha, and their target genes aggravated lipid metabolic disorder in the liver and further accelerated the development of atherosclerosis on a stress of HF diet feeding in AL mice.
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