Abstract

BackgroundAn increasing number of studies have shown that obesity is the key etiological agent of cardiovascular diseases, nonalcoholic fatty liver disease, type 2 diabetes and several kinds of cancer and that gut microbiota change was one of the reasons suffering from obesity. At present, the gut microbiota has gained increased attention as a potential energy metabolism organ. Our recent study reported that cordycepin, a major bioactive component separated from Cordyceps militaris, prevented body weight gain in mice fed a high-fat diet directly acting to adipocytes, however, the effect of cordycepin regulating gut microbiota keeps unknown.MethodsIn this research, we synthesized cordycepin (3-deoxyadenosine) by chemical methods and verified that cordycepin reduces body weight gain and fat accumulation around the epididymis and the kidneys of rats fed a high-fat diet. Furthermore, we used high-throughput sequencing on a MiSeq Illumina platform to test the species of intestinal bacteria in high-fat-diet-induced obese rats.ResultsWe found that cordycepin modifies the relative abundance of intestinal bacteria in high-fat-diet-induced obese rats. However, cordycepin did not alter the variety of bacteria in the intestine. Cordycepin treatment dramatically reversed the relative abundance of two dominant bacterial phyla (Bacteroidetes and Firmicutes) in the high-fat-diet-induced obese rats, resulting in abundance similar to that of the chow diet group.ConclusionOur study suggests that cordycepin can reduce body weight and microbiome done by cordycepin seems be a result among its mechanisms of obesity reduction.

Highlights

  • An increasing number of studies have shown that obesity is the key etiological agent of cardiovascular diseases, nonalcoholic fatty liver disease, type 2 diabetes and several kinds of cancer and that gut microbiota change was one of the reasons suffering from obesity

  • Cordycepin reduced body weight and fat in high-fat-dietinduced obese rats To investigate the effect of cordycepin on body weight and fat, we established the obese rat model by feeding rats a high-fat diet

  • Our results showed that obesity was significantly induced from week 2 to week 4 in rats that were fed a high-fat diet (Fig. 2a)

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Summary

Introduction

An increasing number of studies have shown that obesity is the key etiological agent of cardiovascular diseases, nonalcoholic fatty liver disease, type 2 diabetes and several kinds of cancer and that gut microbiota change was one of the reasons suffering from obesity. The gut microbiota has gained increased attention as a potential energy metabolism organ. Obesity can cause a variety of diseases, such as type 2 diabetes [1], nonalcoholic fatty liver disease, cardiovascular system diseases, insulin resistance, sleep apnea, osteoarthritis, cancer, asthma, and gall-bladder disease [2, 3]. Obese subjects exhibit systemic, chronic inflammation and a high level of serum endotoxins (lipopolysaccharides) that are associated with gut barrier dysfunction [6]. Various mechanisms are reported to have relevance to obesity, including the changes of the locomotor activity, appetite through the pituitary or the hypothalamus in

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