Study On The Mechanism Of Potato Resistant Starch Inhibits Obesity By Modulating The Composition Of Intestinal Microbiota

At present,about one third of the world's people are facing the crisis of obesity and overweight,which is a serious risk to human health.A large number of studies have shown that intestinal microbiota played an important role in the regulation of obesity,and dysbacteriosis will lead to obesity.Improving dietary structure and increasing dietary fiber intake are important methods to regulate intestinal microbiota.The regulatory effect of resistant starch on energy metabolism,glucose and lipid metabolism is one of the hot spots in obesity related fields in recent years.Resistant starch type 3(RS3)is an important functional component of dietary fiber.The mechanism of potato resistant starch RS3(PRS)improving glucose and lipid metabolism and regulating obesity is still unclear.The purpose of this study is to study the effect of PRS on intestinal microbiota abundance and short-chain fatty acids(SCFAs)by simulating human fermentation in vitro;to study the effect of PRS on metabolites in obese mice by using wide target metabonomics technology and reveal its mechanism of improving glucose and lipid metabolism.The research contents and main conclusions are as follows:(1)Based on the method of simulated human gut fermentation in vitro,the effects of PRS on intestinal p H,intestinal microbiota and SCFAs production were investigated.The results showed that 24 h after anaerobic fermentation in vitro,the p H of the medium decreased obviously,the content of SCFAs were significantly increased,The value of Firmicutes/Bacteroidetes(F/B)rate was significantly decreased,and the abundance of Bifidobacterium and Lactobacillus increased significantly,which indicated that PRS could regulate intestinal environment,increase the abundance of probiotics and promote the growth of SCFAs.(2)In order to explore the effect of PRS on glucose and lipid metabolism,C57BL/6 obese mice animal models were established.The results showed that PRS inhibited the weight gain of obese mice induced by high-fat diet in a dose-dependent manner,regulated glucose tolerance(OGTT)and insulin tolerance(ITT)(P < 0.05),significantly reduced the serum triglyceride(TG),total cholesterol(TC)and low-density lipoprotein cholesterol(LDL-C)levels of obese mice,and increased the serum high-density lipoprotein cholesterol(HDL-C)level(P < 0.05),decreased the size of epididymal adipocytes and the ectopic accumulation of lipids in the liver induced by HFD.(3)In order to explore the effect of PRS on intestinal barrier function,C57BL/6 obese mice animal models were established.The results showed that PRS could significantly reduce the body fat rate,serum levels of inflammatory factors such as tumor necrosis factor-?(TNF-?)and interleukin-6(1l-6),reduced the serum level of lipopolysaccharide(LPS),repaired the colon cell damage caused by obesity,promoted the expression of intestinal tight junction protein occludin and ZO-1 in a dose-dependent manner,and significantly promoted the growth of colon cell proliferation and recovery of intestinal barrier function in obese mice.(4)In order to explore the effect of PRS on intestinal microbiota and metabolites,C57BL/6obese mice animal models were established.The results showed that after 12 weeks of continuous intervention,PRS regulated the intestinal microbiota structure of obese mice in a dose-dependent manner.At the phylum level,PRS decreased the F/B rate of intestinal microbiota.At the family level,the abundances of Ruminococcaceae and Lachnospiraceae were decreased,and the abundance of S24-7 was increased.At the genus level,the abundance of Bifidobacterium,Bacteroides,Coprococcus and Ruminococcus were significantly increased.PRS promoted the production of acetic acid and propionic acid.Heat-map representation of the association between fecal metabolites and obesity-related parameters showed that the dominant metabolites acetic acid and propionic acid were negatively correlated with body weight,body fat rate,inflammatory and other obesity-related parameters,and positively correlated with the dominant intestinal microbiota Bifidobacterium,Bacteroides,Coprococcus and Ruminococcus.In conclusion,Bifidobacterium,Bacteroides,Coprococcus and Ruminococcus were dominant microbiota of PRS fermentation,which produced acetic acid and propionic acid and other metabolites,thus regulating glucose and lipid metabolism,intestinal barrier function and intestinal microbiota structure of obese mice,inhibiting obesity.