Dataset Information

High-Fat Diet Induces Dysbiosis of Gastric Microbiota Prior to Gut Microbiota in Association With Metabolic Disorders in Mice.

ABSTRACT: Accumulating evidence suggests that high-fat diet (HFD) induced metabolic disorders are associated with dysbiosis of gut microbiota. However, no study has explored the effect of HFD on the gastric microbiota. This study established the HFD animal model to determine the impact of HFD on the gastric microbiota and its relationship with the alterations of gut microbiota. A total of 40 male C57BL/6 mice were randomly allocated to receive a standard chow diet (CD) or HFD for 12 weeks (12CD group and 12HFD group) and 24 weeks (24CD group and 24HFD group) (n = 10 mice per group). Body weight and length were measured and Lee's index was calculated at different time points. The insulin sensitivity and serum levels of metabolic parameters including blood glucose, insulin and lipid were also evaluated. The gastric mucosa and fecal microbiota of mice were characterized by 16S rRNA gene sequencing. The body weight was much heavier and the Lee's index was higher in 24HFD group than 12HFD. The insulin resistance and serum level of lipid were increased in 24HFD group compared to 12HFD, indicating the aggravation of metabolic disorders as HFD went on. 16S rRNA gene sequencing showed dysbiosis of gastric microbiota with decreased community diversity while no significant alteration in gut microbiota after 12 weeks of HFD. The phyla Firmicutes and Proteobacteria tended to increase whereas Bacteroidetes and Verrucomicrobia decrease in the gastric microbiota of 12HFD mice compared to 12CD. Moreover, a remarkable reduction of bacteria especially Akkermansia muciniphila, which has beneficial effects on host metabolism, was observed firstly in the stomach of 12HFD group and then in the gut of 24HFD group, indicating the earlier alterations of microbiota in stomach than gut after HFD. We also found structural segregation of microbiota in the stomach as well as gut between 12HFD and 24HFD group, which is accompanied by the aggregation of metabolic disorders. These data suggest that HFD affects not only gut microbiota but also gastric microbiota and the disruption of microbial ecosystem in the digestive tract may play a part in the development and progression of metabolic diseases although molecular mechanism requires further investigation.

SUBMITTER: He C

PROVIDER: S-EPMC5900050 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

High-Fat Diet Induces Dysbiosis of Gastric Microbiota Prior to Gut Microbiota in Association With Metabolic Disorders in Mice.

He Cong C Cheng Dandan D Peng Chao C Li Yanshu Y Zhu Yin Y Lu Nonghua N

Frontiers in microbiology 20180409

Accumulating evidence suggests that high-fat diet (HFD) induced metabolic disorders are associated with dysbiosis of gut microbiota. However, no study has explored the effect of HFD on the gastric microbiota. This study established the HFD animal model to determine the impact of HFD on the gastric microbiota and its relationship with the alterations of gut microbiota. A total of 40 male C57BL/6 mice were randomly allocated to receive a standard chow diet (CD) or HFD for 12 weeks (12CD group and ...[more]

PMID: 29686654

Similar Datasets

Project description:High-fat diet (HFD)-induced obesity is a risk factor for many metabolic disorders including cardiovascular diseases, diabetes, and fatty liver disease. Although there are accumulating evidences supporting the assumption that regulating gut microbiota as well as its metabolic status is able to mitigate obesity, the inner relationship between the obesity-related gut microbiota and the relevant metabolites are not well defined. In current study, we applied a traditional herbal formula Kang Shuai Lao Pian (KSLP) to HFD-fed mice and evaluated its effect against obesity. Emphases were addressed on identifying profiles of gut microbiota and fecal metabolites with the aid of 16S rRNA gene sequencing and non-target fecal metabolomics techniques. We showed that KSLP could improve HFD-induced obesity, glucose tolerance disorder, as well as gut dysbiosis. In the gut, KSLP corrected the increased abundance of Firmicutes and Proteobacteria, increased ratio of Firmicutes/Bacteroidetes, and decreased abundance of Bacteroidetes caused by HFD. KSLP also reversed HFD-induced significant changes in the abundance of certain genus including Intestinimonas, Oscillibacter, Christensenellaceae_R-7_group, Ruminococcaceae_UCG-010, and Aliihoeflea. Pearson correlation analysis indicated that except for Ruminococcaceae_UCG-010, other four genera had positive correlations with obesity. In addition, 22 key fecal metabolites responding to KSLP treatment were identified. Pearson correlation analysis showed that those metabolites are intimately related to KSLP effective genera of Intestinimonas, Oscillibacter, and Christensenellaceae_R-7_group. Our results indicate that KSLP is a promising traditional Chinese medicine (TCM) applicable for individuals with HFD habit. Intestinimonas, Oscillibacter, and Christensenellaceae_R-7_group might be responsible for the regulatory effect of KSLP. Linking of obesity phenotypes with gut microbiota as well as fecal metabolites is therefore a powerful research strategy to reveal the mechanism of obesity and the targets of intervention.

Project description:Background: Metabolic syndrome (MS) is one of the major causes of coronary artery diseases (CAD). Gut microbiome diversity and its natural fermentation products are not only correlated with MS and CAD, but their correlations also appear to be stronger than the associations with traditional risk factors. Therefore, the aim of this study was to provide a new potential pathway for the natural fermentation product butyrate to improve MS and to examine whether it is associated with serum metabolic profiles and gut flora composition. Methods: C57BL/6J mice fed a high-fat diet (HFD) were treated with 400 mg/kg of sodium butyrate for 16 weeks. Blood and fecal samples were collected, and the metabolite concentrations and 16s rRNA were measured with liquid chromatography-MS and Illumina platform, respectively. The plasma differential metabolites and gut microbiome composition were analyzed with XCMS online and QIIME 2, respectively. Results: Gut microbiome-derived butyrate reduced glucose intolerance and insulin resistance, resisting HFD-induced increase in the relative abundance of f_Lachnospiraceae, f_Rikenellaceae, and f_Paraprevotellaceae. Meanwhile, sodium butyrate increased the levels of α-linolenate, all-trans-retinal, resolvin E1, and leukotriene in the plasma, and the differential pathways showed enrichment in mainly resolvin E biosynthesis, histidine degradation, lipoxin biosynthesis, and leukotriene biosynthesis. Moreover, sodium butyrate increased the levels of phosphorylated-adenosine 5'-monophosphate-activated protein kinase (p-AMPK) and facilitated glucose transporter member 4 (GLUT4) in the adipose tissue. Conclusion: Butyrate can induce AMPK activation and GLUT4 expression in the adipose tissue, improving cardiovascular disease (CVD)-related metabolic disorder, resisting HFD-induced gut microbiome dysbiosis, and promoting resolvin E1 and lipoxin biosynthesis. Oral supplement of the natural fermentation product butyrate can be a potential strategy for preventing CVD.

Project description:Fat is one of the most important nutrients which provides concentrated energy and essential fatty acids. High fat diet markedly changes the gut microbial composition in mammals, whereas little is known about the impact of fat type on gut microbiome. This study was to evaluate the effects of fat sources on intestinal microbiota of nursery pigs. Eighteen pigs (28 days of age, 8.13 ± 0.10 kg BW) were housed individually (n = 6 per treatment) and allotted to three treatments based on a randomized complete block design. Pigs were fed basal diets with three different fat sources: 6.0% soybean oil (SBO), 6.0% palm oil (PO), and 7.5% encapsulated palm oil (EPO, contains 80% palm oil) respectively. Pigs were euthanized after 28 days of ad libitum feeding, and the digesta in the distal duodenum, jejunum, ileum, cecum and colon of each pig were obtained for microbial composition analysis. Correlation analyses were also performed between microbial composition with nutrients digestibility or growth performance. The results showed that pigs fed PO had marked changes in the bacteria community composition with increasing the richness and diversity in duodenum and jejunum (P < 0.05). Increased abundances of Proteobacteria in duodenum, jejunum and cecum, and decreased abundance of Firmicutes in jejunum were observed in pigs fed PO compared to SBO and EPO. Pigs fed EPO decreased abundances of Proteobacteria in duodenum and jejunum, and increased abundance of Firmicutes compared to pigs fed PO, and was similar to pigs fed SBO. The microbial changes (genus) had significant negative correlation with the fat digestibility. These results indicate that palm oil supplementation in nursery pig diet alters the gut microbial composition, with the most significant changes observed in small intestine. Encapsulation of palm oil, which helps increase the digestibility of palm oil, have beneficial effect on the microbial disturbance caused by palm oil supplementation. Our findings provide a better understanding of how different fat types influence microbial composition in different parts of the intestinal tract and the correlation between bacteria composition and nutrients digestibility, which may provide a new perspective for the rational application of fat in diet.

Project description:High-fat (HF) diet-induced neuroinflammation and cognitive decline in humans and animals have been associated with microbiota dysbiosis via the gut-brain axis. Our previous studies revealed that excretory-secretory products (ESPs) derived from the larval Echinococcus granulosus (E. granulosus) function as immunomodulators to reduce the inflammatory response, while the parasitic infection alleviates metabolic disorders in the host. However, whether ESPs can improve cognitive impairment under obese conditions remain unknown. This study aimed to investigate the effects of E. granulosus-derived ESPs on cognitive function and the microbiota-gut-brain axis in obese mice. We demonstrated that ESPs supplementation prevented HF diet-induced cognitive impairment, which was assessed behaviorally by nest building, object location, novel object recognition, temporal order memory, and Y-maze memory tests. In the hippocampus (HIP) and prefrontal cortex (PFC), ESPs suppressed neuroinflammation and HF diet-induced activation of the microglia and astrocytes. Moreover, ESPs supplementation improved the synaptic ultrastructural impairments and increased both pre- and postsynaptic protein levels in the HIP and PFC compared to the HF diet-treated group. In the colon, ESPs reversed the HF diet-induced gut barrier dysfunction, increased the thickness of colonic mucus, upregulated the expression of zonula occludens-1 (ZO-1), attenuated the translocation of bacterial endotoxins, and decreased the colon inflammation. Notably, ESPs supplementation alleviated the HF diet-induced microbiota dysbiosis. After clarifying the role of antibiotics in obese mice, we found that broad-spectrum antibiotic intervention abrogated the effects of ESPs on improving the gut microbiota dysbiosis and cognitive decline. Overall, the present study revealed for the first time that the parasite-derived ESPs alleviate gut microbiota dysbiosis and improve cognitive impairment induced by a high-fat diet. This finding suggests that parasite-derived molecules may be used to explore novel drug candidates against obesity-associated neurodegenerative diseases.

Dataset Information

High-Fat Diet Induces Dysbiosis of Gastric Microbiota Prior to Gut Microbiota in Association With Metabolic Disorders in Mice.

Publications

High-Fat Diet Induces Dysbiosis of Gastric Microbiota Prior to Gut Microbiota in Association With Metabolic Disorders in Mice.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets