Data · dataset · 2026
Gut microbiome sequencing results in type 2 diabetes under p53 deficiency
Listed in DataCite
The p53 protein has been identified as a critical regulator of metabolic processes in a variety of diseases, including obesity, diabetes, liver disease, and cardiovascular disease.
Description
However, the precise function and mechanism of action of p53 in the regulation of glucose-lipid metabolism through the enterohepatic axis remain to be fully elucidated.The present study investigated the effects of p53 deficiency on type 2 diabetic mice and demonstrated that p53 deficiency resulted in more severe impairment of glucose tolerance and insulin tolerance.
Furthermore, the study revealed that p53 can influence hepatic glucose metabolism via the PI3K/AKT pathway. Additionally, p53 deletion has been observed to modify intestinal function and the intestinal microenvironment, thereby correlating with intestinal function and microbiota composition in T2DM mice. Specifically, p53 knockdown mice exhibited impaired ileal digestion, absorption, and colonic secretion after a HFD (HFD).
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Additionally, the richness and diversity of their intestinal flora were reduced, and these mice exhibited symptoms such as obesity, fat infiltration, defecation abnormalities, and severe abnormalities of glucose and insulin tolerance. The expression levels of β-catenin and c-Myc proteins were found to be elevated in mice fed a HFD, while the expression of these proteins was diminished in mice with p53 knockdown, compared to those on a normal diet.
The experimental results suggest that p53 affects insulin secretion through PI3K/AKT signaling pathway and regulates the distribution of intestinal flora through Wnt signaling pathway, which in turn affects the development of type 2 diabetes mellitus.
Links
Where it is published
- Repository landing page datadryad.org/dataset/doi:10.5061/dryad.2280gb641 ↗
landing page · from DataCite
- DOI doi.org/10.5061/dryad.2280gb641 ↗
DOI / persistent id · from DataCite
Documentation and papers
- Creative Commons Zero v1.0 Universal creativecommons.org/publicdomain/zero/1.0/legalcode ↗
license · from DataCite
Catalogue records · 2
- DataCite API api.datacite.org/dois/10.5061/dryad.2280gb641 ↗
metadata API · from DataCite
- DataCite Commons commons.datacite.org/doi.org/10.5061/dryad.2280gb641 ↗
catalogue entry · from DataCite
Topics
- Inferred from text
- Cardiovascular disease 75% · Disease 75% · Sequencing 75%
Provenance · 1 source records, 11 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| DataCite | 10.5061/dryad.2280gb641 | 7 d ago | JSON v1 |
| Field | Assertion | Extractor | Evidence |
|---|---|---|---|
| access_level | source · DataCite | connector:datacite@1.0.0 | /data/attributes/rightsList |
| byte_size | source · DataCite | connector:datacite@1.0.0 | |
| concepts[disease].local:disease:cardiovascular-disease | enrichment · DataCite | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[disease].local:disease:disease | enrichment · DataCite | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[modality].local:modality:sequencing | enrichment · DataCite | keyword-concept-rules@1.0.0 | title+description (75%) |
| created_date | source · DataCite | connector:datacite@1.0.0 | |
| description | source · DataCite | connector:datacite@1.0.0 | /data/attributes/descriptions |
| license | source · DataCite | connector:datacite@1.0.0 | /data/attributes/rightsList |
| publication_date | source · DataCite | connector:datacite@1.0.0 | /data/attributes/dates |
| title | source · DataCite | connector:datacite@1.0.0 | /data/attributes/titles/0/title |
| version_label | source · DataCite | connector:datacite@1.0.0 |