Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1295124 | ENA |
REPOSITORIES: ENA
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Project description:The brain is a lipid-rich organ, with myelin sheaths containing exceptionally high levels of lipids. Oligodendrocyte dysfunction and myelin lipid deregulation have been implicated in Alzheimer’s disease (AD), yet their precise roles remain unclear. In this study, we examined lipid metabolic alterations, with focus on primary myelin lipids, in AppNL-G-F/NL-G-F (App) AD model mice fed either a normal control diet (NCD) or a high-fat diet (HFD). Brain lipid profiles were altered in App mice, with differential effects depending on diet. Notably, oligodendrocyte gene expression patterns, including those involved in myelin lipid metabolic pathways, were similar between NCD- and HFD-fed App mice and did not correspond with the observed changes in brain lipid composition. This discrepancy indicates that myelin lipid homeostasis in the AD brain is regulated by mechanisms beyond transcriptional control, likely involving post-translational regulation, inter-glial metabolic interactions, and brain-periphery lipid exchange. Importantly, HFD intake did not exacerbate cognitive impairment or neuroinflammation in App mice; rather, HFD-fed App mice showed improved learning during behavioral testing and reduced astrocytic activation. These findings suggest that dietary fat intake does not worsen—and may partially ameliorate—certain aspect of AD pathology, highlighting the complex and context-dependent relationship between metabolic interventions and neurodegenerative disease.
2026-01-25 | GSE304308 | GEO
Project description:Teng-Long-Bu-Zhong-Tang (TLBZT) is a modern anti-cancer herbal formula. Experimental studies have confirmed the anti-cancer potential of TLBZT against colorectal cancer. This trial will evaluate the safety and efficacy of TLBZT based herbal therapy in combination with chemotherapy in patients with metastatic colorectal cancer.
| 2154127 | ecrin-mdr-crc
Project description:Adipose tissue dysfunction results in hepatic lipid overload, driving the progression of liver steatosis and non-alcoholic steatohepatitis. The involvement of adipose tissue-derived small extracellular vesicles (sEVs) in initiating and propagating nonalcoholic fatty liver disease (NAFLD) remains unexplored. Herein, we unveiled that transplanting adipose tissue from high-fat diet (HFD)-fed mice exacerbated insulin resistance and liver steatosis in lean mice, and Sirt3 expression was markedly reduced in adipose tissue from both NAFLD patients and murine NAFLD models. Interestingly, fat-specific Sirt3 overexpression (Sirt3AKI) mice enhanced insulin sensitivity and improved liver steatosis under HFD feeding. Furthermore, adipose tissue-derived sEVs were found to regulate hepatic lipid metabolism in Sirt3AKI mice. In vitro studies demonstrated that Sirt3 overexpressing adipocytes (Sirt3OE) released sEVs to ameliorate lipid accumulation in palmitic acid/oleic acid (P/O)-stimulated hepatocytes. Conversely, sEVs derived from NAFLD patients exacerbated hepatic lipid accumulation in HFD-fed Sirt3AKI mice. MicroRNA sequencing further identified a significant decrease in miR-30a-3p levels in sEVs derived from Sirt3OE adipocytes. Fat-specific miR-30a-3p overexpression worsened hepatic steatosis in HFD-fed Sirt3AKI mice. In contrast, engineered sEVs loaded with miR-30a-3p antagonist or miR-30a-3p inhibition robustly enhanced insulin sensitivity and mitigated hepatic accumulation in HFD-fed mice. Mechanistically, CHIP-qPCR and CHIP-sequencing analyses revealed that Sirt3 suppressed miR-30a-3p transcription through H3K56 acetylation. Dual-luciferase reporter assays validated Beclin1 as a bona fide target mRNA of miR-30a-3p. Taken together, these findings highlight the critical role of exosomal microRNAs in mediating adipocyte-hepatocyte crosstalk, provide novel insights into the mechanisms underlying lipotoxicity in hepatocytes, and suggest miR-30a-3p inhibitor could be a therapeutic agent for NAFLD.
2026-03-02 | GSE307665 | GEO
Project description:Kidney structural integrity is critical for bodily excretory mechanism. Diabetes has been considered as one of the major risk factors for chronic kidney disease, but the underlying mechanism remains elusive. The present study investigates the transcriptomic and proteomic profiling of long-term impact of high-fat diet (HFD) on renal tissue in mice and role of dehydrozingerone (DH) in reinstating the normal kidney function. Animals were divided into four groups- healthy (NCD+Veh), diabetic (HFD-STZ+Veh), healthy+DH (NCD+Veh+DH) and treatment (HFD-STZ+DH). 65th days of HFD-fed C57BL/6 mice developed diabetes and kidney dysfunction evident by albuminuria, proteinuria, and glucotoxicity with accumulation of glucose, triglyceride, cholesterol, albumin, and total protein in blood serum. The HFD-fed kidney showed renal injuries, including prominent defects in the glomerular filtration system by downregulation of proteins involved in transport, metabolic process, energy production, anti-oxidation, etc. Downregulation of lipid metabolism is the most impacted metabolic process under diabetic condition. Downregulation of transport proteins mainly impact the functioning of podocytes, cell adhesion and cytoskeletal rearrangement. HFD feeding also increased oxidative stress and induced mitochondrial dysfunction, and thereby activating the pro-apoptotic pathway. Progression of DNA damage under diabetic condition triggered the epigenetic alteration and subsequent downstream changes which is evident by activation of HDAC1 under diseased condition. Transcriptomic study revealed the potential of dehydrozingerone in attenuating the diabetic condition by positively regulating transport system, mitochondrial function, lipid metabolism, DNA damage and epigenetic alteration, and oxidative stress, which ameliorate the kidney function.
2025-03-01 | GSE290410 | GEO
Project description:Purpose: While various functions of peripheral serotonin are known, the direct role of serotonin in regulating hepatic lipid metabolism in vivo is not well understood. We studied whether serotonin directly acts on liver to regulate lipid metabolism. Methods: Methods: 12 weeks aged liver-specific Htr2a KO (Albumin-Cre+/-; Htr2aflox/flox, herein named Htr2a LKO) mice and wildtype (WT) littermates were fed a high-fat diet (HFD, 60% fat calories) for 8 weeks. Results: Hepatic lipid droplet accumulation, NAFLD activity score, and hepatic triglyceride levels were dramatically reduced in HFD-fed Htr2a LKO mice compared to WT littermates. Conclusions: Gut-derived serotonin is a direct regulator of hepatic lipid metabolism via a gut TPH1-liver HTR2A endocrine axis. And shows promise as a novel drug target to ameliorate NAFLD with minimal systemic metabolic effects.
2018-11-27 | GSE120662 | GEO
Project description:In this project we aimed to investigate the effect of Goreisan (GRS, traditional herbal medicine) on HFpEF model heart failure mouse. HFpEF was induced by administration of high-fat diet (HFD)and N-nitro-L-arginine methyl ester (L-NAME), with or without GRS. Mouse heart proteome was analyzed with LC/MS/MS.
2025-09-02 | PXD049259 | JPOST Repository
Project description:Kurozu is a traditional Japanese rice vinegar. During fermentation and aging of the Kurozu liquid in an earthenware jar over 1 year, solid residue called Kurozu Moromi is produced. In the present study, we evaluated whether concentrated Kurozu or Kurozu Moromi could ameliorate cognitive dysfunction in the senescence accelerated P8 mouse. Senescence accelerated P8 mice were fed 0.25% (w/w) concentrated Kurozu or 0.5% (w/w) Kurozu Moromi for 4 or 25 weeks. Kurozu suppressed cognitive dysfunction and amyloid accumulation in the brain, while Kurozu Moromi showed a tendency to ameliorate cognitive dysfunction, but the effect was not significant. We hypothesize that concentrated Kurozu has an antioxidant effect, however, the level of lipid peroxidation in the brain did not differ in senescence accelerated P8 mice. DNA microarray analysis indicated that concentrated Kurozu increased HSPA1A mRNA expression, a protein that prevents protein misfolding and aggregation. The increase in HSPA1A expression by Kurozu was confirmed using quantitative real-time PCR and immunoblotting methods. Therefore, the suppression of amyloid accumulation by concentrated Kurozu may be associated with HSPA1A induction. However, concentrated Kurozu could not increase HSPA1A expression in mouse primary neurons, suggesting it may not directly affect neurons.
2016-03-11 | GSE70514 | GEO
Project description:We perform scRNA-seq in the livers of C57BL/6 mice fed a CD-HFD for 15 months. Starting from the 13M, mice were treated with FABP5 inhibitor to ameliorate HCC.
2024-02-17 | GSE231818 | GEO
Project description:Samul-tang (SM) is a traditional multi-ingredient treatment widely used in clinical practice for improving ovarian function in women with diminished ovarian reserve. Despite its therapeutic benefits, the complexity of its mechanisms of action due to the combination of multiple compounds has limited its research integration into modern pharmacological science. To address this challenge, we identified 39 herbal compounds as major ingredients in SM and generated transcriptome data from the mice ovaries after administrating with individual ingredients. This dataset aims to provide insights into the mechanisms of action of SM and to aid in the identification of effective ingredient combinations.
2024-04-30 | GSE264002 | GEO