Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 143
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 143
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 209
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 994
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3134
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 574
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 488
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Maternal protein malnutrition leads to liver dysfunction and increases susceptibility to nonalcoholic fatty liver disease in adult fetal growth restriction (FGR) offspring, yet the underlying mechanism remains unknown. Peroxisomes play vital roles in fatty acid β-oxidation (FAO) and detoxification of reactive oxygen species (ROS). Using a well-defined rat model, the peroxins (PEXs), fatty acid metabolic enzymes, and oxidase stress regulators were investigated in the liver of FGR offspring. The results revealed that PEX3, 11b, 14, and 19 were obviously reduced in the fetal liver and lasted to adulthood, suggesting a decrease in the biogenesis and division of peroxisomes. FA metabolism enzymes and ferroptosis regulators were deregulated. To further investigate this association, small interfering RNA was employed to achieve knockdown (KD) of PEX14 in BRL cells (a rat hepatocyte line). PEX14 KD led to dysregulation of PEXs and long-chain FAs accumulation. PEX14 deficiency caused ROS accumulation and lipid peroxidation, finally induced regulated cell death (including apoptosis, autophagy, and ferroptosis). Double knock down (DKD) of PEX14 and fatty acyl-CoA reductase 1 (FAR1) revealed that PEX14 KD-induced ferroptosis was related with enhanced FAR1 level. DKD of PEX14 and Atg5 further confirmed that PEX14 KD-induced cell death was partly autophagy-dependent. Overall, these data demonstrate a vital role for PEX14 in maintaining peroxisome function and liver physiology, and suggest that hepatocyte peroxisome defects partly explain liver dysplasia and lipid metabolism disorders in fetal original liver disease.
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Source |
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http://dx.doi.org/10.1016/j.jnutbio.2023.109432 | DOI Listing |
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