Document Detail


Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs.
MedLine Citation:
PMID:  22094603     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Total parenteral nutrition (TPN) is essential for patients with impaired gut function but leads to parenteral nutrition-associated liver disease (PNALD). TPN disrupts the normal enterohepatic circulation of bile acids, and we hypothesized that it would decrease intestinal expression of the newly described metabolic hormone fibroblast growth factor-19 (FGF19) and also glucagon-like peptides-1 and -2 (GLP-1 and GLP-2). We tested the effects of restoring bile acids by treating a neonatal piglet PNALD model with chenodeoxycholic acid (CDCA). Neonatal pigs received enteral feeding (EN), TPN, or TPN + CDCA for 14 days, and responses were assessed by serum markers, histology, and levels of key regulatory peptides. Cholestasis and steatosis were demonstrated in the TPN group relative to EN controls by elevated levels of serum total and direct bilirubin and also bile acids and liver triglyceride (TG) content. CDCA treatment improved direct bilirubin levels by almost fourfold compared with the TPN group and also normalized serum bile acids and liver TG. FGF19, GLP-1, and GLP-2 were decreased in plasma of the TPN group compared with the EN group but were all induced by CDCA treatment. Intestinal mucosal growth marked by weight and villus/crypt ratio was significantly reduced in the TPN group compared with the EN group, and CDCA treatment increased both parameters. These results suggest that decreased circulating FGF19 during TPN may contribute to PNALD. Moreover, we show that enteral CDCA not only resolves PNALD but acts as a potent intestinal trophic agent and secretagogue for GLP-2.
Authors:
Ajay Kumar Jain; Barbara Stoll; Douglas G Burrin; Jens J Holst; David D Moore
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2011-11-17
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  302     ISSN:  1522-1547     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-04     Completed Date:  2012-02-16     Revised Date:  2013-12-13    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G218-24     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Atrophy
Chenodeoxycholic Acid / administration & dosage,  therapeutic use*
Cholestasis / drug therapy*,  etiology,  pathology
Disease Models, Animal
Fibroblast Growth Factors / metabolism
Glucagon-Like Peptides / metabolism
Intestinal Mucosa / drug effects*,  pathology
Liver Diseases / drug therapy*,  etiology,  pathology
Parenteral Nutrition, Total / adverse effects*
Swine
Treatment Outcome
Grant Support
ID/Acronym/Agency:
P30 DK-56338/DK/NIDDK NIH HHS; P30 DK056338/DK/NIDDK NIH HHS; R01 DK068804/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0GEI24LG0J/Chenodeoxycholic Acid; 62031-54-3/Fibroblast Growth Factors; 62340-29-8/Glucagon-Like Peptides
Comments/Corrections

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