Pleurotus Ostreatus Ameliorates Obesity by Modulating the Gut Microbiota in Obese Mice Induced by High-Fat Diet

Abstract

Pleurotus ostreatus (PO), a common edible mushroom, contains rich nutritional components with medicinal properties. To explore the effect of PO on ameliorating obesity and modulating the gut microbiota, we administered the mice with a low-fat diet or high-fat diet containing different dosages of PO (mass fraction: 0%, 2.5%, 5% and 10%). The body weight, adipose tissue weight, GTT, ITT, blood lipids, serum biomarkers of liver/kidney function, the gut microbiota and function were measured and analyzed after 6 weeks of PO treatment. The results showed PO prevented obesity, maintained glucose homeostasis and beneficially modulated gut microbiota. PO modified the composition and functions of gut microbiota in obese mice and make them similar to those in lean mice, which contributed to weight loss. PO significantly increased the relative abundance of Oscillospira, Lactobacillus group and Bifidobacterium, while decreased the relative abundance of Bacteroides and Roseburia. The prediction of gut microbiota function showed PO upregulated lipid metabolism, carbohydrate metabolism, bile acid biosynthesis, while it downregulated adipocytokine signaling pathway and steroid hormone biosynthesis. Correlation analysis further suggested the potential relationship among obesity, gut microbiota and the function of gut microbiota. In conclusion, all the results indicated that PO ameliorated obesity at least partly by modulating the gut microbiota.

Keywords: 16S rRNA gene; PICRUSt algorithm; Pleurotus Ostreatus; gut microbiota; obesity.

Figure 1

PO prevents HFD-induced obesity in mice. (A) Body weight. * comparison between HFD and LFD, $ comparison between HFD and HFD + POL, # comparison between HFD and HFD + POM, & comparison between HFD and HFD + POH, % comparison between HFD + POL and HFD + POM or HFD + POH. (B) Mass of adipose tissue. (C) Ratio of adipose tissue to body weight. (D) Ratio of organs to body weight. Data are shown as mean ± SEM (n = 8). *, $, #, &, % p < 0.05; **, $$, ##, && p < 0.01.

Figure 2

PO maintains glucose homeostasis and reduces blood lipid level. (A) GTT. (B) Area under curve of GTT. (C) ITT. (D) Area under curve of ITT. (E) Fasting blood glucose. (F) Blood lipid. (A,C) * comparison between HFD and LFD, $ comparison between HFD and HFD + POL, # comparison between HFD and HFD + POM, & comparison between HFD and HFD + POH. Data are shown as mean ± SEM (n = 8). *, $, #, & p < 0.05; **, $$, ##, && p < 0.01.

Figure 3

PO has no obvious harm to the liver and kidney. (A) Liver function biomarker (ALT, AST, ALP). (B) Liver function biomarker (TP, ALB). (C) Kidney function biomarker. Data are shown as mean ± SEM (n = 8). * p < 0.05, ** p < 0.01 compared with HFD.

Figure 4

NMDS analysis, PCA analysis and diversity analysis. (A) NMDS analysis; (B) PCA analysis; (C) Simpson alpha diversity 1-D; (D) Shannon alpha diversity; (E) Bray-Curtis beta diversity. Data are shown as mean ± SEM (n = 6–8). ** p < 0.01 compared with HFD.

Figure 5

PO beneficially modulates the composition of gut microbiota. (A) Microbiota profile at phylum level; (B–M) Correlation analysis between the relative abundance of gut microbiota at phylum level and body weight. Data are shown as mean ± SEM (n = 6–8). * p < 0.05, ** p < 0.01.

Figure 6

LEfSe analysis. (A,B) Biomarker taxa and cladogram between HFD and LFD; (C,D) Biomarker taxa and cladogram between HFD and HFD + POL; (E,F) Biomarker taxa and cladogram between HFD and HFD + POM; (G,H) Biomarker taxa and cladogram between HFD and HFD + POH. n = 6–8.

Figure 7

Gut bacteria at the family level showed significant differences between HFD group and other groups. (A) Venn diagram of increased families in PO treatment groups and LFD compared with HFD; (B) Venn diagram of decreased families in PO treatment groups and LFD compared with HFD; (C–F) The relative abundance of families increased by all of the three PO treatments and LFD; (G–I) The relative abundance of families decreased by all of the three PO treatments and LFD. Data are shown as mean ± SEM (n = 6–8). * p < 0.05, ** p < 0.01.

Figure 8

Gut bacteria at the genus level showed significant differences between HFD group and other groups. (A) Venn diagram of increased genera in PO treatment groups and LFD compared with HFD; (B) Venn diagram of decreased genera in PO treatment groups and LFD compared with HFD; (C–H) The relative abundance of genera increased by all of the three PO treatments and LFD; (I–N) The relative abundance of genera decreased by all of the three PO treatments and LFD. Data are shown as mean ± SEM (n = 6–8). * p < 0.05, ** p < 0.01.

Figure 9

Prediction of gut microbiota function. (A) KEGG pathways increased by PO; (B) KEGG pathways decreased by PO; (C) Spearman’s correlation among body weight, main increased bacteria and increased KEGG pathways; (D) Spearman’s correlation among body weight, main decreased bacteria and decreased KEGG pathways. Data are shown as mean ± SEM (n = 6–8). * p < 0.05, ** p < 0.01.