Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&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
Unlabelled: Apolipoprotein C1 (ApoC1) is a component of multiple lipoproteins where it performs a variety of roles in lipid metabolism and transport. ApoC1 exists as both full-length and truncated isoforms. Truncation of ApoC1 has been postulated to result from the action of dipeptidyl peptidase-4 (DPP-4), the target of a new class of diabetes drugs that includes sitagliptin phosphate. In this study, we sought to determine if oral administration of sitagliptin altered the proportion of ApoC1 isoforms circulating in humans. Results indicated a dramatic change in ApoC1 truncation, consistent with a high level of DPP-4 inhibition by sitagliptin.
Funding: University of Minnesota, Minneapolis, MN, USA.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575309 | PMC |
http://dx.doi.org/10.1007/s13300-015-0123-1 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!