Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fecal microbiota transplantation alleviates diabetes peripheral neuropathy

ABSTRACT: Fecal microbiota transplantation alleviates diabetes peripheral neuropathy

PROVIDER: PRJEB37479 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gut microbiota from healthy donors alleviates peripheral neuropathy in patients with diabetes mellitus

Project description:FMT alleviates peripheral neuropathy in patients with diabetes mellitus

| PRJEB53551 | ENA

Fucoidan reduces NETs accumulation and alleviates chemotherapy-induced peripheral neuropathy

Project description:Fucoidan reduces NETs accumulation and alleviates chemotherapy-induced peripheral neuropathy

| PRJNA1048422 | ENA

Perturbation of spinal cord gene expression accompany peripheral neuropathy in murine model of type 1 diabetes

Project description:Diabetic peripheral neuropathy (DPN) is the most common neurological complication of diabetes. More than 500 differentially expressed genes (DEGs) belonging to multiple functional pathways were identified in diabetic spinal cord and of those the most enriched was RAGE-Diaph1 related PI3K-Akt pathway.

2022-10-16 | E-MTAB-12252 | biostudies-arrayexpress

human gut metagenome

Project description:Fecal microbiota transplantation alleviates diabetes peripheral neuropathy

| PRJDB9649 | ENA

Post-transplant diabetes mellitus after kidney transplantation

Project description:Diabetes mellitus (DM) after transplantation remains a crucial clinical problem in kidney transplantation. To obtain insights into molecular mechanisms underlying the development of post-transplant diabetes mellitus (PTDM) and its early impact on glomerular structures, here we comparatively analyze the proteome of histologically normal appearing glomeruli from patients with PTDM from normoglycemic (NG) transplant recipients, and from recipients with pre-existing type 2 DM (PTDM)

2023-10-24 | PXD042188 | Pride

Dietary folic acid prevents peripheral neuropathy in mouse models of neural tube defects and type 2 diabetes

Project description:Folate-mediated one-carbon metabolism is implicated in several pathologies including neural tube defects (NTDs), cancer and neurodegenerative disorders, whereas diabetes is associated with NTDs and peripheral neuropathy (PN). The development of peripheral neuropathy was assessed in Shmt1+/- and Shmt1 -/- mice, which are models of human folic acid-responsive NTDs, and diabetic (Leprdb) mice to determine if NTDs and PN have a shared etiology. From 6 weeks of age, male and female mice with reduced Shmt1 expression exhibited PN, with greater severity in females compared to males. The neuropathic progression was distinct from diabetic peripheral neuropathy (DPN) observed in Leprdb mice. Excess dietary folic acid prevented PN in both Shmt1-/- and Leprdb/db mice, whereas dietary uridine caused demyelinating PN in mice independent of genotype and folate status. The transcriptome from L3-L5 dorsal root ganglia (DRG) exhibited distinct sex-specific differences in glial cell gene expression when comparing Shmt1+/+ and Shmt1-/- mice. DRG sensory neurons exhibited changes in the expression of solute carriers and ion channels involved in nociception, neurotransmission and structural support. We conclude that reduced thymidylate synthesis causes folic-acid responsive NTDs and PN in mice, and that diabetes sensitizes mice to folic acid-responsive PN. Diabetes induces a special nutritional requirement for high intake of folic acid to prevent PN.

2025-12-17 | GSE275111 | GEO

Transcription profiling of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes

Project description:A study of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes

2006-12-10 | E-MEXP-515 | biostudies-arrayexpress

Expression data from peripheral blood mononuclear cell in patients with type 1 diabetes before and after peripheral stem cell transplantation

Project description:Autologous nonmyeloablative hematopoietic stem cell transplantation (AHST) was the first therapeutic approaches that can improve beta cell function in type 1 diabetic (T1D) patients. This study was designed to investigate the potential mechanisms involved.We applied AHST to nine T1D patients diagnosed within six months and analyzed the acute response in peripheral blood genomic expression profiling at the six-month follow-up. Peripheral blood mononuclear of newly diagnosed type1 diabetes patients at diagnosis and at six months post-transplantation by autologous peripheral stem cell were purified by LymphoprepTm gradient purification according to the manufacturer's instructions (Axis-Shield PoC AS, Oslo, Norway) for futher microarray analysis.

2012-02-20 | E-GEOD-29908 | biostudies-arrayexpress

Fucoidan reduces NETs accumulation and alleviates chemotherapy-induced peripheral neuropathy

Project description:Chemotherapy-induced peripheral neuropathy (CIPN) is a serious adverse reaction of chemotherapy with limited treatment. Previous research indicates neutrophil extracellular traps (NETs) is a critical pathogenesis of CIPN. LPS/HMGB1 serve as important inducers of NETs. Here, we aim to target inhibiting NETs formation (NETosis) to alleviate CIPN. Clinically we found the content of LPS, HMGB1 and NETs in the plasma of CIPN patients was significantly increased and positively correlated with VAS scores. Fucoidan decreased LPS/HMGB1/NETs content and relieved CIPN in mice. Mechanistically, fucoidan upregulated the scavenger receptor A1 (SR-A1) expression and promoted bone marrow derived macrophage (BMDM) to phagocytize LPS/HMGB1. Fucoidan also facilitated BMDM to engulf NETs via the recognition and localization of SR-A1 and HMGB1. The therapeutic effects of fucoidan were abolished by SR-A1 knockout. RNA-seq analysis showed that fucoidan significantly increased sqstm1 (p62) gene expression. Fucoidan promoted the competitive binding of sqstm1 and Nrf2 to Keap1, increasing Nrf2 nuclear translocation and SR-A1 transcription. Additionally, microbial diversity sequencing analysis (16S) showed that fucoidan increased gut microbiota diversity and abundance, and upregulated the Bacteroides/Firmicutes ratio. In conclusion, fucoidan promotes SR-A1-mediated phagocytosis of LPS/HMGB1/NETs and maintains gut microbial homeostasis, providing a potential therapeutic strategy for CIPN.

2025-04-09 | GSE249275 | GEO

Transcriptional profiling of diabetic peripheral neuropathy patients, diabetic patients, and healthy participants

Project description:Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus (DM). It is not diagnosed or managed properly in the majority of patients, because its pathogenesis remains controversial. In this study, using microarray-based genome-wide expression analyses, we sought to identify both common and distinct mechanisms underlying the pathogenesis of DM and DPN. The results demonstrated that down-regulation of the neurotrophin-MAPK signaling pathway may be the major mechanism of DPN pathogenesis, thus providing a potential approach for DPN treatment.

2017-03-09 | GSE95849 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data