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 journalArticlepeer-review

28 Citations (Scopus)
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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

Keywords

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

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