Yeast glucan is a well-known bioactive β-glucan, but it often has different formulations including branched, linear, water-soluble and water-insoluble β-glucans, leading to various experiment data and imperfect mechanism. In this study, we isolated a pure linear β-(1→3) Baker’s yeast glucan (BYGlc), and reported that BYGlc raised glucose uptake in vitro and down-regulated blood glucose and body weight of obese/type 2 diabetic (T2D) mice. It was found that more than 50% FITC-labled BYGlc was directly excreted through the feces, and a small amount of BYGlc was adhered on the intestine epithelium, taken up into the blood circulatory system, and then mainly distributed in liver and spleen. It is interesting that BYGlc in gastrointestinal tract significantly suppressed the expression of sodium-glucose transporter-1 (SGLT-1) on the surface of intestin mucosa to slow down glucose uptake from intestine into blood. Additionally, BYGlc effectively decreased the high level of Firmicutes induced by high-fat diet and increased the proportion of Akkermansia, the top candidate to decrease body weight and improve glucose homeostasis. In liver of T2D mice, BYGlc promoted glycogen synthesis and inhibited lipid accumulation through IRS/Akt pathway. BYGlc also improved the inflammation symptoms indicated by supressing the TNF-a, IL-6 and macrophage infiltration in adipose tissue induced by high-fat diet. Taken together, oral administration of BYGlc has comprehensive benificial effect on gut microbiome, metabolism, inflammation in obese/T2D model, and has a promising application as a drug or food component for preventing or treating obesity/T2D patients.

Yeast β-glucan down-regulates blood glucose level in obesity/type 2 diabetes

251st National Meeting (2016)

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