ArticleEuropean journal of clinical investigation2010
Transgenic overexpression of Abcb11 enhances biliary bile salt outputs, but does not affect cholesterol cholelithogenesis in mice.
Article in European journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Association of Metabolic Syndrome and Cholelithiasis: Understanding the Underlying Mechanism for Better Treatment.Mini reviews in medicinal chemistry · 2026Review
- Sphincter of Oddi Dysfunction Induces Gallstone by Inhibiting the Expression of ABCB11 via PKC-α.Applied biochemistry and biotechnology · 2024Article
- The effect of ursodeoxycholic acid on the relative expression of the lipid metabolism genes in mouse cholesterol gallstone models.Lipids in health and disease · 2020Article
- Hepatic HAX-1 inactivation prevents metabolic diseases by enhancing mitochondrial activity and bile salt export.The Journal of biological chemistry · 2020Article
- Recent Advances in the Critical Role of the Sterol Efflux Transporters ABCG5/G8 in Health and Disease.Advances in experimental medicine and biology · 2020Review
- The arachidonic acid metabolome serves as a conserved regulator of cholesterol metabolism.Cell metabolism · 2014Article
- Clinical application of transcriptional activators of bile salt transporters.Molecular aspects of medicine · 2014Review
- Enhancement of interaction of BSEP and HAX-1 on the canalicular membrane of hepatocytes in a mouse model of cholesterol cholelithiasis.International journal of clinical and experimental pathology · 2014Article
- Puerariae flos alleviates metabolic diseases in Western diet-loaded, spontaneously obese type 2 diabetic model mice.Journal of natural medicines · 2012Article
- Hepatic overexpression of abcb11 promotes hypercholesterolemia and obesity in mice.Gastroenterology · 2011Article
- Biliary cholesterol secretion: more than a simple ABC.World journal of gastroenterology · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCholesterol gallstone disease is a complex genetic trait and induced by multiple but as yet unknown genes. A major Lith gene, Lith1 was first identified on chromosome 2 in gallstone-susceptible C57L mice compared with resistant AKR mice. Abcb11, encoding the canalicular bile salt export pump in the hepatocyte, co-localizes with the Lith1 QTL region and its hepatic expression is significantly higher in C57L mice than in AKR mice. MATERIAL AND
methodsTo investigate whether Abcb11 influences cholesterol gallstone formation, we created an Abcb11 transgenic strain on the AKR genetic background and fed these mice with a lithogenic diet for 56 days.
resultWe excluded functionally relevant polymorphisms of the Abcb11 gene and its promoter region between C57L and AKR mice. Overexpression of Abcb11 significantly promoted biliary bile salt secretion and increased circulating bile salt pool size and bile salt-dependent bile flow rate. However, biliary cholesterol and phospholipid secretion, as well as gallbladder size and contractility were comparable in transgenic and wild-type mice. At 56 days on the lithogenic diet, cholesterol saturation indexes of gallbladder biles and gallstone prevalence rates were essentially similar in these two groups of mice.
conclusionOverexpression of Abcb11 augments biliary bile salt secretion, but does not affect cholelithogenesis in mice.
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