Abstract

Seaweed polysaccharides represent a kind of novel gut microbiota regulator. The advantages and disadvantages of using cecal and fecal microbiota to represent gut microbiota have been discussed, but the regulatory effects of seaweed polysaccharides on cecal and fecal microbiota, which would benefit the study of seaweed polysaccharide-based gut microbiota regulator, have not been compared. Here, the effects of two Sargassum fusiforme polysaccharides prepared by water extraction (SfW) and acid extraction (SfA) on the cecal and fecal microbiota of high-fat diet (HFD) fed mice were investigated by 16S rRNA gene sequencing. The results indicated that 16 weeks of HFD dramatically impaired the homeostasis of both the cecal and fecal microbiota, including the dominant phyla Bacteroidetes and Actinobacteria, and genera Coriobacteriaceae, S24-7, and Ruminococcus, but did not affect the relative abundance of Firmicutes, Clostridiales, Oscillospira, and Ruminococcaceae in cecal microbiota and the Simpson’s index of fecal microbiota. Co-treatments with SfW and SfA exacerbated body weight gain and partially reversed HFD-induced alterations of Clostridiales and Ruminococcaceae. Moreover, the administration of SfW and SfA also altered the abundance of genes encoding monosaccharide-transporting ATPase, α-galactosidase, β-fructofuranosidase, and β-glucosidase with the latter showing more significant potency. Our findings revealed the difference of cecal and fecal microbiota in HFD-fed mice and demonstrated that SfW and SfA could more significantly regulate the cecal microbiota and lay important foundations for the study of seaweed polysaccharide-based gut microbiota regulators.

Highlights

  • The results demonstrated that the high-fat diet (HFD) significantly decreased the abundance of genes encoding α-fucosidase (Figure 4A) and β-glucuronidase (Figure 4G), and increased that of monoresults demonstrated that the HFD significantly decreased the abundance of genes ensaccharide-transporting ATPase (Figure 4B) and β-fructofur-anosidase (Figure 4E) in coding α-fucosidase (Figure 4A) and β-glucuronidase (Figure 4G), and increased that of both the cecal and fecal microbiota, but the alterations of genes encoding α-galactosidase monosaccharide-transporting ATPase (Figure 4B) and β-fructofur-anosidase (Figure 4E) in (Figure 4D) and β-glucosidase (Figure 4F) were only observed in fecal microbiota, and both the cecal and fecal microbiota, but the alterations of genes encoding α-galactosidase that of β-mannosidase (Figure 4H) was only presented in cecal microbiota

  • S. fusiforme

  • We found that the HFD significantly altered the dominant phyla Bacteroidetes and Actinobacteria, and the dominant genera Coriobacteriaceae, S24-7, and Ruminococcus, but did not affect the abundance of Firmicutes, Clostridiales, Oscillospira, and Ruminococcaceae in cecal microbiota and the Simpson’s index of fecal microbiota

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Summary

Introduction

Gut microbiota is a population of microorganisms that colonizes the intestines. This protects against pathogens, provides nutrients, and maintains the integrity of the mucosal barrier, and plays an important role in numerous diseases, such as inflammatory bowel disease, obesity, diabetes mellitus, metabolic syndrome, atherosclerosis, non-alcoholic fatty liver disease, etc. Most studies chose to characterize the gut microbiota composition by sequencing the fecal samples, other than the cecal contents [5,6]. The differences of cecal microbiota and fecal microbiota in mice and human volunteers have been compared by several research groups [7,8,9].

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