The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease.
Adolescent
Adult
Aged
Dietary Supplements
Esters
/ pharmacology
Fatty Acids, Volatile
/ pharmacology
Female
Gastrointestinal Microbiome
/ drug effects
Humans
Inulin
/ pharmacology
Lipid Metabolism
/ drug effects
Liver
/ drug effects
Male
Middle Aged
Non-alcoholic Fatty Liver Disease
/ diet therapy
Propionates
/ pharmacology
Young Adult
clinical trial
dietary intervention
fatty liver
insulin resistance
Journal
Diabetes, obesity & metabolism
ISSN: 1463-1326
Titre abrégé: Diabetes Obes Metab
Pays: England
ID NLM: 100883645
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
16
05
2018
revised:
30
07
2018
accepted:
07
08
2018
pubmed:
12
8
2018
medline:
10
9
2019
entrez:
12
8
2018
Statut:
ppublish
Résumé
The short chain fatty acid (SCFA) propionate, produced through fermentation of dietary fibre by the gut microbiota, has been shown to alter hepatic metabolic processes that reduce lipid storage. We aimed to investigate the impact of raising colonic propionate production on hepatic steatosis in adults with non-alcoholic fatty liver disease (NAFLD). Eighteen adults were randomized to receive 20 g/d of an inulin-propionate ester (IPE), designed to deliver propionate to the colon, or an inulin control for 42 days in a parallel design. The change in intrahepatocellular lipid (IHCL) following the supplementation period was not different between the groups (P = 0.082), however, IHCL significantly increased within the inulin-control group (20.9% ± 2.9% to 26.8% ± 3.9%; P = 0.012; n = 9), which was not observed within the IPE group (22.6% ± 6.9% to 23.5% ± 6.8%; P = 0.635; n = 9). The predominant SCFA from colonic fermentation of inulin is acetate, which, in a background of NAFLD and a hepatic metabolic profile that promotes fat accretion, may provide surplus lipogenic substrate to the liver. The increased colonic delivery of propionate from IPE appears to attenuate this acetate-mediated increase in IHCL.
Identifiants
pubmed: 30098126
doi: 10.1111/dom.13500
pmc: PMC6667894
doi:
Substances chimiques
Esters
0
Fatty Acids, Volatile
0
Propionates
0
inulin-propionate ester
0
Inulin
9005-80-5
Types de publication
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
372-376Subventions
Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/G008272/1
Pays : United Kingdom
Organisme : Department of Health
ID : EME/15/185/16
Pays : United Kingdom
Organisme : Medical Research Council
Pays : United Kingdom
Informations de copyright
© 2018 John Wiley & Sons Ltd.
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