Jiani Wang1, Ruyue Cheng1, Yating Luo1, Qingqing Zhou1, Fengling Jiang1, Xi Shen1, Xiaona Wu2, Fang He1. 1. Department of Nutrition, Food Safety and Toxicology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, China. 2. West China Second University Hospital, Sichuan University, Chengdu 610041, China.
Abstract
OBJECTIVE: To evaluate the possibility of high-fat diet to induce metabolic syndrome and to alter intestinal development, liver function and intestinal microbiotaof C57 BL/6 J mice. METHODS: Total 40 of male C57 BL/6 J aged 3 weeks old were randomly divided into two groups: control group and high-fat diet group. After one week of adaptive feeding, the tested mice in high-fat diet group were fed with high-fat diet for 20 weeks, while those in control group were fed with ordinary diet. During the intervention, the body weight of the tested mice was measured weekly and fasting blood glucose(FBG) was measured monthly. Before the end of the experiment, the oral glucose tolerance test(OGTT) of the tested mice was conducted and the fecal 16 S rRNA sequencing was used to profile fecal microbiota of the test mice. Real-time qPCR was used to analyze the concentration of fecal bifidobacteria. Viscera coefficient of liver, spleen and pancreas, visceral fat-body ratio and intestinal length were measured. The indexes of liver function and the levels of serum lipids, leptin and adiponectin were also measured. Liver inflammation and fat infiltration were observed by anatomical pathological analysis. RESULTS: After intervention of high fat diet, the body weight, FBG, oral glucose tolerance, the fat-body ratio, the levels of serum lipids, leptin and adiponectin of mice were significantly increased(P<0. 05). The inflammatory state of liver and the degree of fat infiltration increased. The length of intestine decreased(P<0. 05). The concentration of Bifidobacterium decreased(P<0. 05), however, the concentration of B. bifidum and B. angulatum increased(P<0. 05). The ACE, Chao1, Shannon and Simpson indexes of the high-fat diet were significantly lower than that of the control group(P<0. 05). Firmicutes, Proteobacteria and Deferribacteres were found significantly more in high-fat diet group(P<0. 05), while Bacteroidetes and Verrucomicrobia were apparently more in control group(P<0. 05). CONCLUSION: High-fat diet could induce the metabolic syndrome in tested C57 BL/6 J, and lead to the damage of intestinal development, abnormality of liver tissue and its function, decrease diversity of intestinal microbiota, and the transformation of intestinal microbiota community to obesity type.
OBJECTIVE: To evaluate the possibility of high-fat diet to induce metabolic syndrome and to alter intestinal development, liver function and intestinal microbiotaof C57 BL/6 J mice. METHODS: Total 40 of male C57 BL/6 J aged 3 weeks old were randomly divided into two groups: control group and high-fat diet group. After one week of adaptive feeding, the tested mice in high-fat diet group were fed with high-fat diet for 20 weeks, while those in control group were fed with ordinary diet. During the intervention, the body weight of the tested mice was measured weekly and fasting blood glucose(FBG) was measured monthly. Before the end of the experiment, the oral glucose tolerance test(OGTT) of the tested mice was conducted and the fecal 16 S rRNA sequencing was used to profile fecal microbiota of the test mice. Real-time qPCR was used to analyze the concentration of fecal bifidobacteria. Viscera coefficient of liver, spleen and pancreas, visceral fat-body ratio and intestinal length were measured. The indexes of liver function and the levels of serum lipids, leptin and adiponectin were also measured. Liver inflammation and fat infiltration were observed by anatomical pathological analysis. RESULTS: After intervention of high fat diet, the body weight, FBG, oral glucose tolerance, the fat-body ratio, the levels of serum lipids, leptin and adiponectin of mice were significantly increased(P<0. 05). The inflammatory state of liver and the degree of fat infiltration increased. The length of intestine decreased(P<0. 05). The concentration of Bifidobacterium decreased(P<0. 05), however, the concentration of B. bifidum and B. angulatum increased(P<0. 05). The ACE, Chao1, Shannon and Simpson indexes of the high-fat diet were significantly lower than that of the control group(P<0. 05). Firmicutes, Proteobacteria and Deferribacteres were found significantly more in high-fat diet group(P<0. 05), while Bacteroidetes and Verrucomicrobia were apparently more in control group(P<0. 05). CONCLUSION: High-fat diet could induce the metabolic syndrome in tested C57 BL/6 J, and lead to the damage of intestinal development, abnormality of liver tissue and its function, decrease diversity of intestinal microbiota, and the transformation of intestinal microbiota community to obesity type.