ArticleThe Journal of biological chemistry2012
Abcb11 deficiency induces cholestasis coupled to impaired β-fatty acid oxidation in mice.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- Liver-directed gene therapy results in amelioration of progressive familial intrahepatic cholestasis type 2 in mice.Hepatology communications · 2026Article
- Calculus Bovis ameliorates primary sclerosing cholangitis via a dual-pronged mechanism restoring bile acid and lipid homeostasis in the gut-liver axis.Chinese medicine · 2026Article
- ATP-binding Cassette Transporter Defects and Their Roles in Hepatic Diseases.Journal of clinical and translational hepatology · 2026Review
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- Gestational hypercholanemia suppresses pregnancy-associated adipose mass increase and stimulates a pro-inflammatory environment in mice.Physiological reports · 2024Article
- Medaka liver developed Human NAFLD-NASH transcriptional signatures in response to ancestral bisphenol A exposure.Research square · 2024Article
- Sex-specific expression of the human NAFLD-NASH transcriptional signatures in the liver of medaka with a history of ancestral bisphenol A exposure.bioRxiv : the preprint server for biology · 2024Article
- Dynamics of blood Taurine concentration and its correlation with nutritional and physiological status during the fattening period of Japanese black cattle.Journal of animal science · 2024Article
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- Synthesis of Methylgenipin and Evaluation of Its Anti-Hepatic Injury Activity.Molecules (Basel, Switzerland) · 2023Article
- Developmental programming: Preconceptional and gestational exposure of sheep to a real-life environmental chemical mixture alters maternal metabolome in a fetal sex-specific manner.The Science of the total environment · 2023Article
- A Dual Coverage Monitoring of the Bile Acids Profile in the Liver-Gut Axis throughout the Whole Inflammation-Cancer Transformation Progressive: Reveal Hepatocellular Carcinoma Pathogenesis.International journal of molecular sciences · 2023Article
- Resistance to energy metabolism - targeted therapy of AML cells residual in the bone marrow microenvironment.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Gene Therapy for Acquired and Genetic Cholestasis.Biomedicines · 2022Review
- Recent updates on progressive familial intrahepatic cholestasis types 1, 2 and 3: Outcome and therapeutic strategies.World journal of hepatology · 2022Review
- Paeoniae Radix Rubra can enhance fatty acid β-oxidation and alleviate gut microbiota disorder in α-naphthyl isothiocyanate induced cholestatic model rats.Frontiers in pharmacology · 2022Article
- An Integrated Proteomics and Metabolomics Strategy for the Mechanism of Calcium Oxalate Crystal-Induced Kidney Injury.Frontiers in medicine · 2022Article
- Role of FXR in Bile Acid and Metabolic Homeostasis in NASH: Pathogenetic Concepts and Therapeutic Opportunities.Seminars in liver disease · 2021Review
- iTRAQ-based quantitative proteomics analysis of the hepatoprotective effect of melatonin on ANIT-induced cholestasis in rats.Experimental and therapeutic medicine · 2021Article
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12 authors.
Funding
Abstract
The bile salt export pump (BSEP) is an ATP-binding cassette transporter that serves as the primary system for removing bile salts from the liver. In humans, deficiency of BSEP, which is encoded by the ABCB11 gene, causes severe progressive cholestatic liver disease from early infancy. In previous studies of Abcb11 deficiency in mice generated on a mixed genetic background, the animals did not recapitulate the human disease. We reasoned that ABCB11 deficiency may cause unique changes in hepatic metabolism that are predictive of liver injury. To test this possibility, we first determined that Abcb11 knock-out (KO) C57BL/6J mice recapitulate human deficiency. Before the onset of cholestasis, Abcb11 KO mice have altered hepatic lipid metabolism coupled with reduced expression of genes important in mitochondrial fatty acid oxidation. This was associated with increased serum free-fatty acids, reduced total white adipose, and marked impairment of long-chain fatty acid β-oxidation. Importantly, metabolomic analysis confirmed that Abcb11 KO mice have impaired mitochondrial fatty acid β-oxidation with the elevated fatty acid metabolites phenylpropionylglycine and phenylacetylglycine. These metabolic changes precede cholestasis but may be of relevance to cholestatic disease progression because altered fatty acid metabolism can enhance reactive oxygen species that might exacerbate cholestatic liver damage.
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