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Iron overload reduces synthesis and elimination of bile acids in rat liver
A. Prasnicka, H. Lastuvkova, F. Alaei Faradonbeh, J. Cermanova, M. Hroch, J. Mokry, E. Dolezelova, P. Pavek, K. Zizalova, L. Vitek, P. Nachtigal, S. Micuda,
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 2011
Free Medical Journals
od 2011
Nature Open Access
od 2011-12-01
PubMed Central
od 2011
Europe PubMed Central
od 2011
ProQuest Central
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Health & Medicine (ProQuest)
od 2011-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2011
Springer Nature OA/Free Journals
od 2011-12-01
- MeSH
- biologické markery MeSH
- cholesterol metabolismus MeSH
- exprese genu MeSH
- játra metabolismus patologie MeSH
- krysa rodu rattus MeSH
- messenger RNA genetika metabolismus MeSH
- modely nemocí na zvířatech MeSH
- oxidační stres MeSH
- přetížení železem etiologie metabolismus patologie MeSH
- žlučové kyseliny a soli metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Excessive iron accumulation in the liver, which accompanies certain genetic or metabolic diseases, impairs bile acids (BA) synthesis, but the influence of iron on the complex process of BA homeostasis is unknown. Thus, we evaluated the effect of iron overload (IO) on BA turnover in rats. Compared with control rats, IO (8 intraperitoneal doses of 100 mg/kg every other day) significantly decreased bile flow as a consequence of decreased biliary BA secretion. This decrease was associated with reduced expression of Cyp7a1, the rate limiting enzyme in the conversion of cholesterol to BA, and decreased expression of Bsep, the transporter responsible for BA efflux into bile. However, IO did not change net BA content in faeces in response to increased intestinal conversion of BA into hyodeoxycholic acid. In addition, IO increased plasma cholesterol concentrations, which corresponded with reduced Cyp7a1 expression and increased expression of Hmgcr, the rate-limiting enzyme in de novo cholesterol synthesis. In summary, this study describes the mechanisms impairing synthesis, biliary secretion and intestinal processing of BA during IO. Altered elimination pathways for BA and cholesterol may interfere with the pathophysiology of liver damage accompanying liver diseases with excessive iron deposition.
Citace poskytuje Crossref.org
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- $a Prasnicka, Alena $u Department of Pharmacology, Charles University, Faculty of Medicine in Hradec Kralove, Hradec Kralove, Czech Republic. Department of Biological and Medical Sciences, Charles University, Faculty of Pharmacy in Hradec Kralove, Hradec Kralove, Czech Republic.
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- $a Excessive iron accumulation in the liver, which accompanies certain genetic or metabolic diseases, impairs bile acids (BA) synthesis, but the influence of iron on the complex process of BA homeostasis is unknown. Thus, we evaluated the effect of iron overload (IO) on BA turnover in rats. Compared with control rats, IO (8 intraperitoneal doses of 100 mg/kg every other day) significantly decreased bile flow as a consequence of decreased biliary BA secretion. This decrease was associated with reduced expression of Cyp7a1, the rate limiting enzyme in the conversion of cholesterol to BA, and decreased expression of Bsep, the transporter responsible for BA efflux into bile. However, IO did not change net BA content in faeces in response to increased intestinal conversion of BA into hyodeoxycholic acid. In addition, IO increased plasma cholesterol concentrations, which corresponded with reduced Cyp7a1 expression and increased expression of Hmgcr, the rate-limiting enzyme in de novo cholesterol synthesis. In summary, this study describes the mechanisms impairing synthesis, biliary secretion and intestinal processing of BA during IO. Altered elimination pathways for BA and cholesterol may interfere with the pathophysiology of liver damage accompanying liver diseases with excessive iron deposition.
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