DIET-HYGIENE
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB13041 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1313800_1.fastq.gz | Fastqsanger.gz | |||
| ERR1313800_2.fastq.gz | Fastqsanger.gz | |||
| ERR1313810_1.fastq.gz | Fastqsanger.gz | |||
| ERR1313810_2.fastq.gz | Fastqsanger.gz | |||
| ERR1313801_1.fastq.gz | Fastqsanger.gz |
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Project description:Carotenoids are naturally occurring pigments in plants responsible for the orange, yellow, and red color of fruits and vegetables. Carrots are one of the primary dietary sources of carotenoids. The biological activities of carotenoids in higher organisms are well documented in most tissues but not the large intestine. The gastrointestinal barrier acts as a line of defense against the systemic invasion of pathogenic bacteria, especially at the colonic level. Proteins involved in tight junction assembly between epithelial cells and mucus secretion from goblet cells are essential for maintaining intestinal barrier homeostasis. A high-fat diet can cause gut impairment by inducing barrier permeability, leading to low-grade chronic inflammation via metabolic endotoxemia. Our hypothesis for this study is that the dietary intake of carotenoid-rich foods can alleviate obesity-associated gut inflammation and strengthen the intestinal barrier function. Male C57BL/6J mice were randomized to one of four experimental diets for 20 weeks (n = 20 animals/group): Low-fat diet (LFD, 10% calories from fat), high-fat diet (HFD, 45% calories from fat), HFD with white carrot powder (HFD + WC), or HFD with orange carrot powder (HFD + OC). Colon tissues were harvested to analyze the biochemical effects of carotenoids in carrots. The distal sections were subjected to isobaric labeling-based quantitative proteomics in which tryptic peptides were labeled with tandem mass tags, followed by fractionation and LC-MS/MS analysis in an Orbitrap Eclipse Tribrid instrument. High-performance liquid chromatography results depicted that the HFD+WC pellets were carotenoid-deficient, and the HFD+OC pellets contained high concentrations of provitamin A carotenoids, specifically α-carotene and β-carotene. As a result of the quantitative proteomics, a total of 4410 differentially expressed proteins were identified. Intestinal barrier-associated proteins were highly upregulated in the HFD+OC group, particularly mucin-2 (MUC-2). Upon closer investigation into mucosal activity, other proteins related to MUC-2 functionality and tight junction management were upregulated by the HFD+OC dietary intervention. Carotenoid-rich foods may prevent high-fat diet-induced intestinal barrier disruption by promoting colonic mucus synthesis and secretion in mammalian organisms.
2024-11-04 | PXD054150 | Pride
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.
2024-03-20 | GSE261887 | GEO
Project description:Purpose: To identify the impact of thermoneutral housing as opposed to standard housing on gene expression profiles in the mouse peripheral blood mononuclear cells (PBMCs), focusing on proinflammatory immune responses and high-fat diet induced non-alcoholic fatty liver disease pathogenesis. Methods: Expression profiles from PBMCs collected from C57Bl6 mice fed chow or high-fat diet for 8 weeks, following 2 weeks at either standard or thermoneutral housing conditions. Sequencing was performed in duplicate, the Illumina HiSeq 2500. Transcripts that passed quality filters were analyzed at the gene level, using Strand NGS for accurate alignment and quantification. Results: We mapped approximately 20million reads per sample to the mm10 genome using annotations produced by Ensembl, which represented 36186 transcripts. Approximately 14000 genes exhibited reasonable expression in at least one experimental condition. The primary focus was the effect of housing temperature while holding diet consistent (i.e. thermoneutral vs standard, both on high-rat diet), where ~2700 genes exhibited differential regulation. Conclusions: We present the transcriptomic profile of PBMCs from mice fed chow of high-fat diets, following either standard or thermoneutral housing. We obseve an augmented proinflammatory immune response.
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Project description:Currently, it is an open question how gut senses metabolic alterations and whether this is transmitted to other tissues via EVs. Here, we observed that protein packaging in gut derived EVs (GDE) from a diet induced-prediabetic mouse mode, specifically small intestine, is increased in prediabetes. Proteins related to lipid metabolism and to oxidative stress management were more abundant in prediabetic GDE compared to healthy controls. Low-fat diet: A1 to A3 high-fat diet: A4 to A6
2022-04-04 | PXD028338 | Pride
Project description:To investigate the effects of diabetic conditions on the development of AD pathology, we fed wild-type and Alzheimer's disease model (App[NL-F/NL-F]) mice with control or high fat diet from 6 months after birth for 12 months, then examined behavior, brain pathology and gene expression profiles. Both groups of mice fed with high fat diet exhibited diabetic conditions, and App[NL-F/NL-F] mice exhibited aggravated cognitive impairment with enhanced Alzheimer's disease pathology.
2021-06-30 | GSE152539 | GEO
Project description:The objective of the experiment was to dissect the effects of a high-fat diet on juvenile adipose tissue gene expression under conditions of excess calorie intake versus normal calorie intake in comparison to a standard low-fat diet. For this purpose juvenile mice were fed (A) a standard low-fat diet (CD), (B) a high-fat diet ad libitum (excess calorie intake) (HFD) and (C) a high-fat diet with calorie consumption restricted to the calorie consumption of the CD diet (R-HFD). RNA expression was profiled after 1 week of feeding in the periuterine fat depot.
2019-04-09 | E-MTAB-7755 | biostudies-arrayexpress
Project description:This study was performed to investigate the effect of aging and high fat diet on gut microbiota in F344 rats by the pyrosequencing method.
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Project description:A number of studies have proposed that excess food intake, particularly of high fat diets arise due dysregulation of homeostatic mechanisms regulating neuroendocrine control of appetite and energy balance. Current dogma suggests high fat diets invoke hypothalamic inflammation which reduces hypothalamic sensitivity to metabolic and hormonal cues of conveying peripheral status of energy balance, such as leptin and insulin. A hypothesis for the mechanism leading to hypothalamic inflammation is based on high fat diet mediated changes in gut microbiota which are then proposed to increase circulating levels of lipopolysaccharide (LPS). This in turn activates a hypothalamic inflammatory response via the toll-like receptor (TLR4) and CD14. The aim of this study was to determine hypothalamic gene expression in response to long term feeding of a high fat diet, taking into account the importance of using a control diet with a similar composition and balanced for sucrose content.
2018-10-23 | E-MTAB-6929 | biostudies-arrayexpress
Project description:We investigated remodeling of the mitochondrial proteome to determine mechanisms of changes to lipid oxidation following high-fat feeding. C57BL/6J mice consumed either a high-fat diet (HFD, 60% fat) or low fat diet (LFD, 10% fat) for 12 weeks. Mice were fasted 4 hours then anaesthetized by sodium pentobarbital for tissue collection. A mitochondrial-enriched fraction was prepared from gastrocnemius muscles and underwent proteomic analysis by high-resolution mass spectrometry.
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Project description:High Fat Diet Experiment SD rats fed either an AIN93G-based low fat diet or an AIN93G-based high fat diet. Keywords: ordered
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