Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs. / Jain, Ajay Kumar; Stoll, Barbara; Burrin, Douglas G; Holst, Jens Juul; Moore, David D.

In: American Journal of Physiology: Gastrointestinal and Liver Physiology, Vol. 302, No. 2, 2012, p. G218-24.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Jain, AK, Stoll, B, Burrin, DG, Holst, JJ & Moore, DD 2012, 'Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs', American Journal of Physiology: Gastrointestinal and Liver Physiology, vol. 302, no. 2, pp. G218-24. https://doi.org/10.1152/ajpgi.00280.2011

APA

Jain, A. K., Stoll, B., Burrin, D. G., Holst, J. J., & Moore, D. D. (2012). Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs. American Journal of Physiology: Gastrointestinal and Liver Physiology, 302(2), G218-24. https://doi.org/10.1152/ajpgi.00280.2011

Vancouver

Jain AK, Stoll B, Burrin DG, Holst JJ, Moore DD. Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs. American Journal of Physiology: Gastrointestinal and Liver Physiology. 2012;302(2):G218-24. https://doi.org/10.1152/ajpgi.00280.2011

Author

Jain, Ajay Kumar ; Stoll, Barbara ; Burrin, Douglas G ; Holst, Jens Juul ; Moore, David D. / Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs. In: American Journal of Physiology: Gastrointestinal and Liver Physiology. 2012 ; Vol. 302, No. 2. pp. G218-24.

Bibtex

@article{2527884ac9a648e5acc6818dab63d9e3,
title = "Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs",
abstract = "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.",
keywords = "Animals, Animals, Newborn, Atrophy, Chenodeoxycholic Acid, Cholestasis, Disease Models, Animal, Fibroblast Growth Factors, Glucagon-Like Peptides, Intestinal Mucosa, Liver Diseases, Parenteral Nutrition, Total, Swine, Treatment Outcome",
author = "Jain, {Ajay Kumar} and Barbara Stoll and Burrin, {Douglas G} and Holst, {Jens Juul} and Moore, {David D}",
year = "2012",
doi = "10.1152/ajpgi.00280.2011",
language = "English",
volume = "302",
pages = "G218--24",
journal = "American Journal of Physiology: Gastrointestinal and Liver Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Enteral bile acid treatment improves parenteral nutrition-related liver disease and intestinal mucosal atrophy in neonatal pigs

AU - Jain, Ajay Kumar

AU - Stoll, Barbara

AU - Burrin, Douglas G

AU - Holst, Jens Juul

AU - Moore, David D

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

KW - Animals

KW - Animals, Newborn

KW - Atrophy

KW - Chenodeoxycholic Acid

KW - Cholestasis

KW - Disease Models, Animal

KW - Fibroblast Growth Factors

KW - Glucagon-Like Peptides

KW - Intestinal Mucosa

KW - Liver Diseases

KW - Parenteral Nutrition, Total

KW - Swine

KW - Treatment Outcome

U2 - 10.1152/ajpgi.00280.2011

DO - 10.1152/ajpgi.00280.2011

M3 - Journal article

VL - 302

SP - G218-24

JO - American Journal of Physiology: Gastrointestinal and Liver Physiology

JF - American Journal of Physiology: Gastrointestinal and Liver Physiology

SN - 0193-1857

IS - 2

ER -

ID: 38433067