Impact of Plant-Based Dietary Fibers on Metabolic Homeostasis in High-Fat Diet Mice via Alterations in the Gut Microbiota and Metabolites

The gut microbiota contributes to metabolic disease, and diet shapes the gut microbiota, emphasizing the need to better understand how diet impacts metabolic disease via gut microbiota alterations. Fiber intake is linked with improvements in metabolic homeostasis in rodents and humans, which is associated with changes in the gut microbiota. However, dietary fiber is extremely heterogenous, and it is imperative to comprehensively analyze the impact of various plant-based fibers on metabolic homeostasis in an identical setting and compare the impact of alterations in the gut microbiota and bacterially derived metabolites from different fiber sources. The objective of this study is to analyze the impact of different plant-based fibers (pectin, beta-glucan, wheat dextrin, resistant starch, and cellulose as a control) on metabolic homeostasis through alterations in the gut microbiota and its metabolites in high-fat diet (HFD)-fed mice. HFD-fed mice were supplemented with 5 different fiber types (pectin, beta-glucan, wheat dextrin, resistant starch, or cellulose as a control) at 10% (w/w) for 18 weeks (n=12/group), measuring body weight, adiposity, indirect calorimetry, glucose tolerance, and the gut microbiota and metabolites. Only beta-glucan supplementation during HFD-feeding decreased adiposity and body weight gain and improved glucose tolerance compared to HFD-cellulose, while all other fibers had no effect. This was associated with increased energy expenditure and locomotor activity in mice compared to HFD-cellulose. All fibers supplemented into a HFD uniquely shifted the intestinal microbiota and cecal short-chain fatty acids, however only beta-glucan supplementation increased cecal butyrate levels. Lastly, all fibers altered the small intestinal microbiota and portal bile acid composition. These findings demonstrate that beta-glucan consumption is a promising dietary strategy for metabolic disease, possibly via increased energy expenditure through alterations in the gut microbiota and bacterial metabolites in mice.