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: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.
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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.
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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:RNA sequencing in Atp7b -/- mice under high-fat diet conditions
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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.
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Project description:Type 2 diabetic cardiomyopathy (DCM) has been linked to Ca2+ signaling alterations, notably a decreased mitochondrial Ca2+ uptake. Uncovering of Ca2+ microdomains between cardiac mitochondria and reticulum launched a new investigation avenue for cardiometabolic diseases. We here aimed to study if the impairment of mitochondrial Ca2+ handling could be due to a dysregulation of the reticulum-mitochondria interactions or of the mitochondrial Ca2+ uniporter in the diabetic mice heart. Phenotypic alterations of the type 2 diabetic mouse heart, was done using an in vivo obesogenic high fat high sucrose diet fed mouse model (HFHSD: 20% proteins, 36% lipids). The composition of the cardiac MAM fractions between standard diet-fed (SD) mice and HFHSD (HF) mice at 16 weeks was analysed by MS-based quantitative proteomics.
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Project description:Mice livers: high fat diet versus high fat diet (HF) supplemented with pirfenidone (HFP)
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