Abstract
Various dietary fibers are considered to prevent obesity by modulating the gut microbiota. Cordyceps sinensis polysaccharide (CSP) is a soluble dietary fiber known to have protective effects against obesity and related diseases, but whether these effects induce any side effects remains unknown. The function and safety of CSP were tested in high-fat diet (HFD)-feding C57BL/6J mice. The results revealed that even though CSP supplementation could prevent an increase in body weight, it aggravated liver fibrosis and steatosis as evidenced by increased inflammation, lipid metabolism markers, insulin resistance (IR) and alanine aminotransferase (ALT) in HFD-induced obesity. 16S rDNA gene sequencing was used to analyze the gut microbiota composition, and the relative abundance of the Actinobacteria phylum, including the Olsenella genus, was significantly higher in CSP-treated mice than in HFD-fed mice. CSP supplementation may increase the proportion of Actinobacteria, which can degrade CSP. The high level of Actinobacteria aggravated the disorder of the intestinal flora and contributed to the progression from obesity to nonalcoholic steatohepatitis (NASH) and related diseases.
Highlights
Obesity, which is characterized by metabolic disorder and chronic low-grade inflammation, has become a widespread public health problem [1, 2]
After comparing the weight of epididymal fat and the size of adipocytes (Fig 2C and 2E) in the high-fat diet (HFD) and HFD+Cordyceps sinensis polysaccharide (CSP) groups, we found that the weight of epididymal fat in the HFD+CSP group was remarkably lower than that in the HFD group (P
Liver hematoxylin and eosin (H&E) staining (Fig 2F) revealed severe fibrosis, steatohepatitis changes and increased infiltration of inflammatory cells around the central vein of hepatocytes in the mice in the HFD+CSP group compared with the HFD group
Summary
Obesity, which is characterized by metabolic disorder and chronic low-grade inflammation, has become a widespread public health problem [1, 2]. The excessive accumulation of fat and dyslipidemia can increase the risk of type 2 diabetes, nonalcoholic fatty liver disease (NAFLD) and even liver cancer [3, 4]. Multiple factors contribute to the development of obesity, including energy consumption, high fat intake and the microbiome. Over the past few years, numerous studies have demonstrated that the gut microbiota plays an important role in diet-induced obesity and related diseases [5,6,7]. Research on animal models has demonstrated that some specific intestinal microorganisms could prevent diet-induced obesity.
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