The gut-liver axis

R.G.J. Visschers, M.D.P. Luyer, F.G. Schaap, S. Olde Damink, P.B. Soeters*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


PURPOSE OF REVIEW: The liver adaptively responds to extra-intestinal and intestinal inflammation. In recent years, the role of the autonomic system, intestinal failure and gut microbiota has been investigated in development of hepatic, intestinal and extra-intestinal disease. RECENT The autonomic nervous system can be stimulated via enteral fat leading cholecystokinin release, stimulating receptors in the gut and in the promotes bowel integrity, dampening the inflammatory response to food Consensus exists that intravenously administered long-chain fatty acids liver damage but randomized-controlled trials are lacking. Disruption of enterohepatic circulation of bile salts can give rise to cholestasis and nonalcoholic fatty liver disease, which may progress to fibrosis and Reduced intestinal availability of bile salts reduces stimulation of the farnesoid X receptor. This may induce hepatic bile salt overload and hepatotoxicity through reduced action of intestinal fibroblast growth Evidence is put forward to suggest that the intestinal microbiota is with liver abnormalities. SUMMARY: Enteral lipids reduce inflammation damage during stress or systemic inflammation, whereas parenteral lipid associated with liver damage. Maintaining the enterohepatic circulation salts limits hepatic cholestasis through an farnesoid X receptor pathway. Changes in gut microbiota composition may induce liver disease.
Original languageEnglish
Pages (from-to)576-581
JournalCurrent Opinion in Clinical Nutrition and Metabolic Care
Issue number5
Publication statusPublished - 1 Jan 2013

Cite this