The consequences of trehalose intake on brain metabolism in mice
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ABSTRACT:
PROVIDER: PRJNA449666 | ENA |
REPOSITORIES: ENA
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Project description:In the present study, we investigated the consequences of trehalose intake on brain metabolism in mice drinking for 0, 1, and 10 days. Microarray analyses were performed to identify the molecular targets involved in the brain metabolism of trehalose intake.
2019-04-01 | GSE112976 | GEO
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Project description:Systemic Consequences of Chronic Ethanol Intake: From Microbiome Shifts to Metabolic Impairment
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Project description:Clostridioides difficile, the leading cause of antibiotic-associated diarrhoea worldwide, is a genetically diverse species which can metabolise a number of nutrient sources upon colonising a dysbiotic gut environment. Trehalose, a disaccharide sugar consisting of two glucose molecules bonded by an α 1,1-glycosidic bond, has been hypothesised to be involved in the emergence of C. difficile hypervirulence due to its increased utilisation by the RT027 and RT078 strains. Using RNA-sequencing analysis, we report the identification of a putative trehalose metabolism pathway which is induced during growth in trehalose: this has not been previously described within the C. difficile species. These data demonstrate the metabolic diversity exhibited by C. difficile which warrants further investigation to elucidate the molecular basis of trehalose metabolism within this important gut pathogen.
2023-05-26 | GSE232033 | GEO
Project description:Chronic ethanol (EtOH) consumption is a major contributor to multi-organ dysfunction, yet its systemic effects remain incompletely understood. To address this, we utilized a physiologically relevant long-term mouse model, administering 20% EtOH in drinking water for 60 weeks, to investigate the integrated consequences of chronic exposure. EtOH-consuming mice (0.4-0.5 mL/day) exhibited >30% reductions in both chow and fluid intake, resulting in a 12% decrease in total caloric intake compared to controls (P<0.001). Body mass remained similar until week 52, after which EtOH-treated mice had lower body mass due to reductions in both lean and fat mass (P≤0.004). Functional assessments revealed impaired treadmill endurance (-17%) and grip strength (-11%) (P≤0.037), while motor coordination remained unaffected (P=0.203). Chronic EtOH exposure significantly altered gut microbiota composition, reducing Lactobacillus and enriching Faecalibaculum, Clostridium, and Bifidobacterium at the genus level. These changes were accompanied by marked depletion of short-chain fatty acids (P≤0.05). Indirect markers of gut permeability (serum LPS & zonulin) and liver injury (serum ALT & AST, hepatic amyloid content) were elevated, alongside increased total cholesterol and >62% upregulation of hepatic TNFα, IL-6 & serum amyloid A (P≤0.046). EtOH also induced dyslipidemia and glucose intolerance (P≤0.041), although transcriptomic changes in white adipose tissue were minimal despite elevated free fatty acids. In conclusion, chronic EtOH consumption disrupts energy balance, compromises gut barrier integrity, and impairs hepatic metabolism, collectively driving systemic and metabolic dysfunction. These findings underscore the gut-liver axis as a key mediator of EtOH-induced pathology and highlight the gut microbiome as a promising therapeutic target.
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Project description:Grapevine is an important economic fruit tree, and European grape (Vitis vinifera L.) has been widely used in fresh food, drying, winemaking and grape seed extract. However, most European grapes have low resistance to low temperature, drought and salt stress, and these abiotic stresses will limit the growth and development of grapes, thereby affecting the grape quality and yield. Many reports have shown that exogenous or endogenous trehalose can help improve plant stress resistance. Therefore, in order to investigate the function and molecular mechanism of trehalose metabolism in grape response to stress, this project was conducted.
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Project description:Trehalose is the nonreducing disaccharide of glucose, evolutionarily conserved in invertebrates. The living skin equivalent (LSE) is an organotypic coculture containing keratinocytes cultivated on fibroblast-populated dermal substitutes. We demonstrated that human primary fibroblasts treated with highly concentrated trehalose promote significantly extensive spread of the epidermal layer of LSE without any deleterious effects. The RNA-seq analysis of trehalose-treated 2D and 3D fibroblasts at early time points revealed the involvement of the CDKN1A pathway, the knockdown of which significantly suppressed the upregulation of DPT, ANGPT2, VEGFA, EREG, and FGF2. The trehalose-treated fibroblasts were positive for senescence-associated β-galactosidase. Finally, transplantation of the dermal substitute with trehalose-treated fibroblasts accelerated wound closure and increased capillary formation significantly in the experimental mouse wounds in vivo, which was canceled by the CDKN1A knockdown. These data indicate that high-concentration trehalose can induce the senescence-like state in fibroblasts via CDKN1A/p21, which may be therapeutically useful for optimal wound repair.
2023-01-10 | GSE184892 | GEO
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Project description:Abrupt weaning imposes highly variable physiological stress on pigs, yet the mechanisms underlying this variability remain poorly understood. We applied an integrative approach combining transcriptomics, gastrointestinal phenotyping, and blood biomarkers to characterize gut–brain axis dynamics at one week post‑weaning (day 7) and at the end of the nursery phase (day 39) in pigs with divergent early performance. Twenty‑four pigs of similar weaning weight (5.65 ± 1.0 kg) were selected from pens showing extreme early feed intake post-weaning and subsequently classified by average daily gain (ADG) as a proxy for individual feed intake (n = 12/timepoint). RNA sequencing of ileal and hypothalamic tissue revealed that low‑ADG pigs at day 7 exhibited impaired intestinal barrier function, suppressed metabolic and immune pathways, and hypothalamic activation of appetite‑suppressing (mTORC1, GLP‑1) and thermogenic signalling, together with endocrine disruption. By day 39, digestive and metabolic pathways were upregulated in the ileum of low‑ADG pigs, yet gut integrity deficits persisted alongside sustained hypothalamic immune activation and disrupted appetite signalling. Blood profiles indicated prolonged metabolic imbalance, characterized by elevated triglycerides, insulin, leptin, and TNF‑α, and reduced PYY. Collectively, these findings define a “low feed intake syndrome”, in which early nutrient deprivation, compromised gut integrity, and dysregulated neuroendocrine signalling converge to perpetuate poor growth and long‑term maladaptation.
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