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, Catriona Tedford, Jimmy D Bell, Louise Thomas, Arne N Akbar, Natalie E Riddell, Rohini Sharma, Mark R Thursz, Pinelopi Manousou, Gary Frost

Journal: Diabetes, obesity & metabolism 2019;21(2):372-376

PMID: 30098126

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Non-alcoholic fatty liver disease (NAFLD) is characterised by an accumulation of fat within the liver, and is strongly associated with obesity. Recent investigations suggest that diet, the gut microbiota and liver fat storage could be linked through a mechanism involving short chain fatty acids (SCFA), in particular the SCFA propionate, which are produced by the gut bacteria. The aim of this randomised controlled study was to evaluate whether an inulin-propionate ester (IPE) has benefits in patients with NAFLD. Subjects with NAFLD received either 20 g/d of inulin (control) or IPE for 42 days. 18 subjects completed the trial. Intrahepatocellular lipids IHCL (a marker of fat accumulation in the liver) increased post supplementation in both groups with no significant difference between control and IPE group. There was a change in insulin resistance (HOMA-IR) which was significantly different between groups, with a non-significant increase in the inulin-control group and decrease in the IPE group. There were no within- or between-group differences in body composition. The authors discuss these unexpected results and suggest that the SCFA acetate, from inulin fermentation by gut bacteria, may have led to an increase in IHCL which was attenuated by the propionate.

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 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.

© 2018 John Wiley & Sons Ltd.

Address: Section for Nutrition Research, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, UK.; Stable Isotope Biochemistry Laboratory, Scottish Universities Environmental Research Centre, University of Glasgow, Glasgow, UK.; School of Science, University of the West of Scotland, Hamilton, UK.; Department of Life Sciences, Faculty of Science and Technology, Research Centre for Optimal Health, University of Westminster, London, UK.; Division of Infection and Immunity, University College London, London, UK.; Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK.; Department of Surgery and Cancer, Imperial College London, London, UK.; Liver Unit, St Mary's Hospital, Imperial College NHS Trust, London, UK.

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