Type 2 diabetes mellitus (T2DM) may lead to abnormally elevated blood glucose, lipid metabolism disorder, and low-grade inflammation. Besides, the development of T2DM is always accompanied by gut microbiota dysbiosis and metabolic dysfunction. In this study, the T2DM mice model was established by feeding a high-fat/sucrose diet combined with injecting a low dose of streptozotocin. Additionally, the effects of oral administration of ethanol extract from Sanghuangporous vaninii (SVE) on T2DM and its complications (including hypoglycemia, hyperlipidemia, inflammation, and gut microbiota dysbiosis) were investigated. The results showed SVE could improve body weight, glycolipid metabolism, and inflammation-related parameters. Besides, SVE intervention effectively ameliorated the diabetes-induced pancreas and jejunum injury. Furthermore, SVE intervention significantly increased the relative abundances of Akkermansia, Dubosiella, Bacteroides, and Parabacteroides, and decreased the levels of Lactobacillus, Flavonifractor, Odoribacter, and Desulfovibrio compared to the model group (LDA > 3.0, p < 0.05). Metabolic function prediction of the intestinal microbiota by PICRUSt revealed that glycerolipid metabolism, insulin signaling pathway, PI3K-Akt signaling pathway, and fatty acid degradation were enriched in the diabetic mice treated with SVE. Moreover, the integrative analysis indicated that the key intestinal microbial phylotypes in response to SVE intervention were strongly correlated with glucose and lipid metabolism-associated biochemical parameters. These findings demonstrated that SVE has the potential to alleviate T2DM and its complications by modulating the gut microbiota imbalance.
Alcoholic liver damage is caused by long-term drinking, and it further develops into alcoholic liver diseases. In this study, we prepared a probiotic fermentation product of Grifola frondosa total active components (PFGF) by fermentation with Lactobacillus acidophilus, Lactobacillus rhamnosus, and Pediococcus acidilactici. After fermentation, the total sugar and protein content in the PFGF significantly decreased, while the lactic acid level and antioxidant activity of the PFGF increased. Afterward, we investigated the alleviating effect of PFGF on alcoholic liver injury in alcohol-fed mice. The results showed that the PFGF intervention reduced the necrosis of the liver cells, attenuated the inflammation of the liver and intestines, restored the liver function, increased the antioxidant factors of the liver, and maintained the cecum tissue barrier. Additionally, the results of the 16S rRNA sequencing analysis indicated that the PFGF intervention increased the relative abundance of beneficial bacteria, such as Lactobacillus, Ruminococcaceae, Parabacteroids, Parasutterella, and Alistipes, to attenuate intestinal inflammation. These results demonstrate that PFGF can potentially alleviate alcoholic liver damage by restoring the intestinal barrier and regulating the intestinal microflora.
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