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.
Highlights
Non-alcoholic fatty liver disease (NAFLD), a condition characterized by the accumulation of fat within the liver, is regarded as a major risk factor in the development of type 2 diabetes.[1]
To augment colonic propionate production we have developed an inulin-propionate ester (IPE), whereby the short chain fatty acids (SCFA) propionate is bound to the dietary fibre inulin, which is released through microbial hydrolysis in the colon.[9]
Inulin was chosen as a positive control to account for any effects that may derive from fermentation of this substrate by the gut microbiota
Summary
Non-alcoholic fatty liver disease (NAFLD), a condition characterized by the accumulation of fat within the liver, is regarded as a major risk factor in the development of type 2 diabetes.[1] The prevalence of NAFLD is strongly associated with obesity,[1] current guidelines for the prevention and management of NAFLD are based solely on body weight loss through diet and exercise.[1] While lifestyle wileyonlinelibrary.com/journal/dom. Recent investigations suggest that diet, the gut microbiota and liver fat storage could be linked through a mechanism involving short chain fatty acids (SCFA), the major products of dietary fibre fermentation in the colon. These volunteers were identified as having NAFLD on the basis of an elevated intrahepatocellular lipid (IHCL) content from magnetic resonance imaging
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