Ontology highlight
ABSTRACT:
PROVIDER: PRJNA843192 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19440700.fastq.gz | Fastqsanger.gz | |||
| SRR19440700_1.fastq.gz | Fastqsanger.gz | |||
| SRR19440700_2.fastq.gz | Fastqsanger.gz | |||
| SRR19440701_1.fastq.gz | Fastqsanger.gz | |||
| SRR19440701_2.fastq.gz | Fastqsanger.gz |
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Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
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Project description:The chicken gastrointestinal tract (GIT) harbours a complex microbial community, involved in several physiological processes such as host immunomodulation and feed digestion. Other studies were already performed to define the chicken gut metagenome and its fecal metaproteome. For the first time, the present study analysed dietary effects on the protein inventory of the microbiota in crop and ceca of broilers. We performed quantitative label-free metaproteomics by using 1D-gel electrophoresis coupled with LC-MS/MS to identify the structural and functional changes triggered by diets supplied with varying amount of mineral phosphorus (P) and microbial phytase (MP). Phylogenetic assessment based on label-free quantification (LFQ) values of the proteins identified Lactobacillaceae as the major family in the crop section regardless of the diet, whereas proteins belonging to the family Veillonellaceae increased with the P supplementation. Within the ceca section, proteins of Bacteroidaceae were more abundant in the P-supplied diets, whereas proteins of Eubacteriaceae decreased with the P-addition. Proteins of the Ruminococcaceae increasedraised with the amount of MP while proteins of Lactobacillaceae werewas more abundant in the MP-lacking diets. Classification of the identified proteins into COGs and KEGG pathways underlined a diverse microbiota activity depending on the dietary regimen, indicating a thriving microbial community in the case of P and MP supplementation, and stressed microbial community when no P and MP were supplied. Insights oninto the identified KEGG pathways, as well as comparison between the GIT sections, dietary treatments, and the bacterial families encoding for the pathways of interest are provided. T) harbours a complex microbial community, involved in several physiological processes such as host immunomodulation and feed digestion. Other studies were already performed to define the chicken gut metagenome and its fecal metaproteome. For the first time, the present study analysed dietary effects on the protein inventory of the microbiota in crop and ceca of broilers. We performed quantitative label-free metaproteomics by using 1D-gel electrophoresis coupled with LC-MS/MS to identify the structural and functional changes triggered by diets supplied with varying amount of mineral phosphorus (P) and microbial phytase (MP). Phylogenetic assessment based on label-free quantification (LFQ) values of the proteins identified Lactobacillaceae as the major family in the crop section regardless of the diet, whereas proteins belonging to the family Veillonellaceae increased with the P supplementation. Within the ceca section, proteins of Bacteroidaceae were more abundant in the P-supplied diets, whereas proteins of Eubacteriaceae decreased with the P-addition. Proteins of the Ruminococcaceae increasedraised with the amount of MP while proteins of Lactobacillaceae werewas more abundant in the MP-lacking diets. Classification of the identified proteins into COGs and KEGG pathways underlined a diverse microbiota activity depending on the dietary regimen, indicating a thriving microbial community in the case of P and MP supplementation, and stressed microbial community when no P and MP were supplied. Insights oninto the identified KEGG pathways, as well as comparison between the GIT sections, dietary treatments, and the bacterial families encoding for the pathways of interest are provided.
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