The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease

Edward S. Chambers, Claire S. Byrne, Annette Rugyendo, Douglas J. Morrison, Tom Preston, M. Catriona Tedford, Jimmy D. Bell, E. Louise Thomas, Arne N. Akbar, Natalie E. Riddell, Rohini Sharma, Mark R. Thursz, Pinelopi Manousou, Gary Frost

Research output: Contribution to journalArticle

8 Downloads (Pure)

Abstract

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 randomised to receive 20g/day 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 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.
Original languageEnglish
Pages (from-to)372-376
Number of pages5
JournalDiabetes, Obesity and Metabolism
Volume21
Issue number2
Early online date11 Aug 2018
DOIs
Publication statusPublished - 28 Feb 2019

Fingerprint

Inulin
Propionates
Dietary Supplements
Esters
Lipids
Volatile Fatty Acids
Liver
Fermentation
Metabolome
Dietary Fiber
Colon
Acetates
Fats
Non-alcoholic Fatty Liver Disease

Keywords

  • clinical trial
  • dietary intervention
  • fatty liver
  • insulin resistance

Cite this

Chambers, Edward S. ; Byrne, Claire S. ; Rugyendo, Annette ; Morrison, Douglas J. ; Preston, Tom ; Tedford, M. Catriona ; Bell, Jimmy D. ; Thomas, E. Louise ; Akbar, Arne N. ; Riddell, Natalie E. ; Sharma, Rohini ; Thursz, Mark R. ; Manousou, Pinelopi ; Frost, Gary. / The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease. In: Diabetes, Obesity and Metabolism. 2019 ; Vol. 21, No. 2. pp. 372-376.
@article{aa67cddd839e47cc9786b27f2a166681,
title = "The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease",
abstract = "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 randomised to receive 20g/day 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 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.",
keywords = "clinical trial, dietary intervention, fatty liver, insulin resistance",
author = "Chambers, {Edward S.} and Byrne, {Claire S.} and Annette Rugyendo and Morrison, {Douglas J.} and Tom Preston and Tedford, {M. Catriona} and Bell, {Jimmy D.} and Thomas, {E. Louise} and Akbar, {Arne N.} and Riddell, {Natalie E.} and Rohini Sharma and Thursz, {Mark R.} and Pinelopi Manousou and Gary Frost",
year = "2019",
month = "2",
day = "28",
doi = "10.1111/dom.13500",
language = "English",
volume = "21",
pages = "372--376",
journal = "Diabetes, Obesity and Metabolism",
issn = "1463-1326",
publisher = "Wiley",
number = "2",

}

Chambers, ES, Byrne, CS, Rugyendo, A, Morrison, DJ, Preston, T, Tedford, MC, Bell, JD, Thomas, EL, Akbar, AN, Riddell, NE, Sharma, R, Thursz, MR, Manousou, P & Frost, G 2019, 'The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease' Diabetes, Obesity and Metabolism, vol. 21, no. 2, pp. 372-376. https://doi.org/10.1111/dom.13500

The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease. / Chambers, Edward S.; Byrne, Claire S.; Rugyendo, Annette; Morrison, Douglas J.; Preston, Tom; Tedford, M. Catriona; Bell, Jimmy D.; Thomas, E. Louise; Akbar, Arne N.; Riddell, Natalie E.; Sharma, Rohini; Thursz, Mark R.; Manousou, Pinelopi; Frost, Gary.

In: Diabetes, Obesity and Metabolism, Vol. 21, No. 2, 28.02.2019, p. 372-376.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease

AU - Chambers, Edward S.

AU - Byrne, Claire S.

AU - Rugyendo, Annette

AU - Morrison, Douglas J.

AU - Preston, Tom

AU - Tedford, M. Catriona

AU - Bell, Jimmy D.

AU - Thomas, E. Louise

AU - Akbar, Arne N.

AU - Riddell, Natalie E.

AU - Sharma, Rohini

AU - Thursz, Mark R.

AU - Manousou, Pinelopi

AU - Frost, Gary

PY - 2019/2/28

Y1 - 2019/2/28

N2 - 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 randomised to receive 20g/day 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 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.

AB - 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 randomised to receive 20g/day 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 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.

KW - clinical trial

KW - dietary intervention

KW - fatty liver

KW - insulin resistance

U2 - 10.1111/dom.13500

DO - 10.1111/dom.13500

M3 - Article

VL - 21

SP - 372

EP - 376

JO - Diabetes, Obesity and Metabolism

JF - Diabetes, Obesity and Metabolism

SN - 1463-1326

IS - 2

ER -