Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
infection has been associated with the development of insulin resistance (IR). This study aimed to examine the effect of -derived extracellular vesicles (EVs) on IR induction. EVs were derived from two strains, and characterised by transmission electron microscopy and dynamic light scattering. Different concentrations of insulin were added to HepG2 cells to induce IR model. HepG2 cells were exposed to various concentrations of -derived EVs to assess IR development. The gene expression of , , , , , and miR-140 was examined using RT-qPCR. Glucose uptake analysis revealed insulin at 5 × 10 mol/l and EVs at 50 µg/ml induced IR model in HepG2 cells. -derived EVs downregulated the expression level of , , and , and upregulated , , , and miR-140 expression in HepG2 cells. In conclusion, our findings propose a novel mechanism by which derived EVs could potentially induce IR.
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Source |
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http://dx.doi.org/10.1080/13813455.2024.2418494 | DOI Listing |
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