Abstract

Gut microbiota is closely related to type 2 diabetes mellitus (T2DM). The gut microbiota of patients with T2DM is significantly different from that of healthy subjects in terms of bacterial composition and diversity. Here, we used the fermentation products of Paenibacillus bovis sp. nov. BD3526 to study the disease progression of T2DM in Goto-kakisaki (GK) rats. We found that the symptoms in GK rats fed the fermentation products of BD3526 were significantly improved. The 16S rRNA sequencing showed that the fermentation products of BD3526 had strong effects on the gut microbiota by increasing the content of Akkermansia. In addition, the interaction of the genus in the gut of the BD3526 group also significantly changed. Additional cytokine detection revealed that the fermentation products of BD3526 can reduce the inflammatory factors in the intestinal mucus of GK rats and thereby inhibit the inflammatory response and ameliorate the symptoms of T2DM.

Highlights

  • According to data published by the International Diabetes Federation, there were 425 million people with diabetes worldwide in 2017

  • The results demonstrated that postprandial blood glucose in the BD3526 group showed a significant decrease in the fourth and fifth week (∗P-value < 0.05, mean ± SEM) (Figure 1B)

  • In the body mass index test, we subtracted the body weight of the control group rats from that of the BD3526 group and observed that the weight gain rate of GK rats in the BD3526 group was significantly lower than that in the control group (Figure 1D). These results indicate that the BD3526 strain fermentation products had the ability to reduce diabetes-related indicators in GK rats of Type 2 diabetes mellitus (T2DM)

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Summary

Introduction

According to data published by the International Diabetes Federation, there were 425 million people with diabetes worldwide in 2017. Type 2 diabetes mellitus (T2DM) is characterized by a sustained decrease in the insulin secretion of pancreatic β-cells, which leads to insufficient insulin to fulfill the requirement of the body. Long-term T2DM in the human body can cause serious complications, for example in the kinds of kidney disease, cancer and cardiovascular disease (Stern, 1995; Coughlin et al, 2004). In the last two decades, evidence has accumulated that the pathogenesis of T2DM and its complications may be related to inflammation factors (i.e., IL-1β, IL-6, MCP-1, TNF-α and IFNγ) (Cuman et al, 2001; Rotter et al, 2002; Masters et al, 2010; Westwellroper et al, 2011; WestwellRoper et al, 2014; Greer et al, 2016). Excess IL-6 promotes pancreatic islet β lymphocyte differentiation and overexpresses the IgG gene, which promotes excessive activation of T lymphocytes and thereby

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