Abstract

Obesity and the related liver diseases are prevalent around the world. Although probiotics have been shown to prevent obesity through multiple ways, only few researches investigated the lipid-lowering effects of probiotic Bacillus. Moreover, the limited results consistently suggested that Bacillus regulated genes related to lipogenesis and oxidation, but no further exploration was made. Our previous study revealed that Bacillus amyloliquefaciens SC06 has a potent antioxidant capacity in vitro. The aim of this study is to investigate the effects of SC06 on obesity and the associated liver injury of high-fat diet (HFD)-fed-mice and its underlying mechanism. By feeding normal chow (NC), NC+SC06, HFD, and HFD+SC06 to mice, we found that SC06 improved body weight gain, hepatic steatosis, and glucose metabolism of HFD-mice. Furthermore, SC06 also increased the antioxidant capacity of mice through Nrf2/Keap1 signaling pathway. High-throughput sequencing of 16S rRNA gene showed that HFD changed the gut microbiota dramatically, while HFD+SC06 decreased the ratio of Firmicutes/Bacteroidetes and increased TM7 abundance. More differences were also found in lower taxa. Altogether, SC06 is a potential probiotic that decreases HFD-related lipid accumulation and liver injury via regulating the antioxidant capacity and host gut microbiota.

Highlights

  • With more than 1.4 billion overweight or obese adults (Hall et al, 2015), obesity has become a major threat to public health in both developed and developing countries (Haslam and James, 2005)

  • Histological analysis of perirenal, subcutaneous and epididymal adipose tissues showed that the size of adipocytes in the high-fat diet (HFD) group was greater than that in normal chow (NC), but the size of adipocytes in the HFD+SC06 group was less than that in HFD group (Figures 1D–F)

  • HFD significantly increased glucose levels during the Oral glucose tolerance test (OGTT) (p < 0.05, Figure 1G), and HFD+SC06 elevated the clearance of glucose slightly

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Summary

Introduction

With more than 1.4 billion overweight or obese adults (Hall et al, 2015), obesity has become a major threat to public health in both developed and developing countries (Haslam and James, 2005). The mean BMI in Chinese adults increased from 22.7 kg/m2 in Bacillus Improve Host Liver Injury. Obesity and obesity-related metabolic diseases are caused by multiple factors, including diet, gene, environment and mentality (Kopelman, 2000). Associated with obesity, non-alcoholic fatty liver disease (NAFLD) is the major reason for abnormal liver function worldwide (Li et al, 2014). Multiple possible sources of oxidant stress in the fatty liver may constitute the “second hit” for cellular injury in nonalcoholic steatohepatitis (Carmiel-Haggai et al, 2004). It is believed that antioxidants may be effective agents in treating active steatohepatitis through attenuating the secondary injury. Foster et al (2011) found that antioxidant atorvastatin combined with vitamin C and E was effective in reducing the hepatic steatosis in individuals with NAFLD. S-adenosylmethionine, which generates glutathione (GSH), had the potential to treat NAFLD (Musso et al, 2013)

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