Abstract
The role of dietary fibre and short-chain fatty acids (SCFA) in obesity development is controversially discussed. Here, we investigated how various types of dietary fibre and different SCFA ratios affect metabolic syndrome-related disorders. Male mice (B6) were fed high-fat diets supplemented with dietary fibres (either cellulose, inulin or guar gum) or different Ac:Pr ratios (high acetate (HAc) or propionate (HPr)) for 30 weeks. Body-fat gain and insulin resistance were greatly reduced by inulin, but not by guar gum, and completely prevented by SCFA supplementation. Only inulin and HAc increased body temperature, possibly by the induction of beige/browning markers in WAT. In addition, inulin and SCFA lowered hepatic triglycerides and improved insulin sensitivity. Both, inulin and HAc reduced hepatic fatty acid uptake, while only inulin enhanced mitochondrial capacity and only HAc suppressed lipogenesis in liver. Interestingly, HPr was accompanied by the induction of Nrg4 in BAT. Fermentable fibre supplementation increased the abundance of bifidobacteria; B. animalis was particularly stimulated by inulin and B. pseudolongum by guar gum. We conclude that in contrast to guar gum, inulin and SCFA prevent the onset of diet-induced weight gain and hepatic steatosis by different mechanisms on liver and adipose tissue metabolism.
Highlights
Low dietary fibre consumption in Western countries is accompanied by an increased prevalence of obesity and insulin resistance[1, 2]
short-chain fatty acids (SCFA) supplementation resulted in a reduced body-weight gain and final body weight compared to the HF-group no matter whether a high Ac or a high Pr ratio was applied (Fig. 1B,C)
In accordance with total body fat data (Table 1), the HF diet-induced increase of subcutaneous and epididymal white adipose tissue weight was attenuated by inulin and completely prevented by Ac/Pr, but not by guar gum supplementation (Fig. 1J,K)
Summary
Low dietary fibre consumption in Western countries is accompanied by an increased prevalence of obesity and insulin resistance[1, 2]. One postulated mechanism relates to the production of short-chain fatty acids (SCFA), mainly acetate (Ac) and propionate (Pr) These SCFA are formed from dietary fibre as a result of intestinal fermentation. There were no effects on body weight/fat, inulin supplementation increased SCFA formation and reduced the Ac:Pr ratio in caecal contents and portal vein plasma. Based on these results we hypothesised that prolonged inulin supplementation might repress the onset of diet-induced obesity and related disorders, such as hepatic steatosis and insulin resistance. We assume that depending on the fibre type, various total SCFA amounts and different Ac:Pr ratios are formed which in turn could be responsible for the controversial literature data regarding dietary fibre effects on obesity. We examined the intestinal microbiota composition in faecal samples
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