Effect of bile acid supplementation on endogenous lipid synthesis in patients with short bowel syndrome: A pilot study.


Journal

Clinical nutrition (Edinburgh, Scotland)
ISSN: 1532-1983
Titre abrégé: Clin Nutr
Pays: England
ID NLM: 8309603

Informations de publication

Date de publication:
03 2020
Historique:
received: 15 04 2018
revised: 18 01 2019
accepted: 26 03 2019
pubmed: 20 4 2019
medline: 20 8 2021
entrez: 20 4 2019
Statut: ppublish

Résumé

Short bowel syndrome patients (SBS) receiving parenteral nutrition (PN) often have dyslipidaemia and can develop intestinal failure-associated liver disease (IFALD). These patients demonstrate increased cholesterol synthesis and hepatic lipogenesis. These lipid disturbances may be due to a decreased concentration of the bile acid pool or malabsorption. The aim of this pilot study was to evaluate the effect of bile acid administration on lipid synthesis in patients with SBS. The 24 h fractional synthesis rate (FSR) of cholesterol and triglycerides was measured by the isotopic method (deuterated water) before and after 4 months of ursodeoxycholic acid (UDCA) treatment (20 mg/kg/day). Five short bowel patients (age: 53.4 ± 19.2 years) who had normal liver function and lipid plasmatic profiles received 1920 ± 300 ml of PN for 151 ± 74 days (mean PN energy intake was 27.0 ± 6.0 kcal/kg body weight, composed with 3.87 ± 1.38 g/kg of carbohydrate, 0.72 ± 0.25 g/kg of fat and 1.10 ± 0.23 g/kg of amino acids). Plasma metabolites, liver enzymes, 7-α-OH-cholesterol and steatosis levels were also evaluated before and after treatment. Student's t-tests were performed, and the results were expressed in means (±SD). After treatment, decreases in the absolute values of cholesterol synthesis (0.31 ± 0.12 mmol L In SBS patients, UDCA decreases the hepatic synthesis of triglycerides and cholesterol. These results suggest that UDCA could prevent the onset of the IFALD.

Sections du résumé

BACKGROUND & AIMS
Short bowel syndrome patients (SBS) receiving parenteral nutrition (PN) often have dyslipidaemia and can develop intestinal failure-associated liver disease (IFALD). These patients demonstrate increased cholesterol synthesis and hepatic lipogenesis. These lipid disturbances may be due to a decreased concentration of the bile acid pool or malabsorption. The aim of this pilot study was to evaluate the effect of bile acid administration on lipid synthesis in patients with SBS.
METHODS
The 24 h fractional synthesis rate (FSR) of cholesterol and triglycerides was measured by the isotopic method (deuterated water) before and after 4 months of ursodeoxycholic acid (UDCA) treatment (20 mg/kg/day). Five short bowel patients (age: 53.4 ± 19.2 years) who had normal liver function and lipid plasmatic profiles received 1920 ± 300 ml of PN for 151 ± 74 days (mean PN energy intake was 27.0 ± 6.0 kcal/kg body weight, composed with 3.87 ± 1.38 g/kg of carbohydrate, 0.72 ± 0.25 g/kg of fat and 1.10 ± 0.23 g/kg of amino acids). Plasma metabolites, liver enzymes, 7-α-OH-cholesterol and steatosis levels were also evaluated before and after treatment. Student's t-tests were performed, and the results were expressed in means (±SD).
RESULTS
After treatment, decreases in the absolute values of cholesterol synthesis (0.31 ± 0.12 mmol L
CONCLUSIONS
In SBS patients, UDCA decreases the hepatic synthesis of triglycerides and cholesterol. These results suggest that UDCA could prevent the onset of the IFALD.

Identifiants

pubmed: 31000340
pii: S0261-5614(19)30151-7
doi: 10.1016/j.clnu.2019.03.037
pii:
doi:

Substances chimiques

Bile Acids and Salts 0
Triglycerides 0
Cholesterol 97C5T2UQ7J

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

928-934

Informations de copyright

Copyright © 2019 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Auteurs

Thomas Mouillot (T)

Hepatology and Gastroenterology Department, University Hospital F. Mitterrand, F-21000, Dijon, France; Centre for Taste and Feeding Behaviour, CNRS, INRA, University of Bourgogne Franche-Comté, F-21000, Dijon, France.

Michel Beylot (M)

Neurocardiology Unit - EA 4612, Institute of Pharmaceutical and Biological Sciences, University Claude Bernard Lyon 1, Lyon, France.

Jocelyne Drai (J)

Biochemistry and Molecular Biology Unit, Hospices Civil de Lyon, F-69495, Pierre Benite Cedex, France.

Patrick Hillon (P)

Hepatology and Gastroenterology Department, University Hospital F. Mitterrand, F-21000, Dijon, France.

Patrick Gelas (P)

Nutrition Intensive Care Unit, Hospices Civil de Lyon, F-69495, Pierre Benite Cedex, France.

Madeleine Lauverjat (M)

Nutrition Intensive Care Unit, Hospices Civil de Lyon, F-69495, Pierre Benite Cedex, France.

Laurent Brondel (L)

Hepatology and Gastroenterology Department, University Hospital F. Mitterrand, F-21000, Dijon, France; Centre for Taste and Feeding Behaviour, CNRS, INRA, University of Bourgogne Franche-Comté, F-21000, Dijon, France.

Cécile Chambrier (C)

Nutrition Intensive Care Unit, Hospices Civil de Lyon, F-69495, Pierre Benite Cedex, France. Electronic address: cecile.chambrier@chu-lyon.fr.

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Classifications MeSH