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: 3122
Function: getPubMedXML
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
The growing worldwide burden of insulin resistance (IR) emphasizes the importance of early identification for improved management. Obesity, particularly visceral obesity, has been a key contributing factor in the development of IR. The obesity-associated chronic inflammatory state contributes to the development of obesity-related comorbidities, including IR. Adipocytokines, which are released by adipose tissue, have been investigated as possible indicators of IR. Visfatin was one of the adipocytokines that attracted attention due to its insulin-mimetic activity. It is released from a variety of sources, including visceral fat and macrophages, and it influences glucose metabolism and increases inflammation. The relationship between visfatin and IR in obesity is debatable. As a result, the purpose of this review was to better understand the role of visfatin in glucose homeostasis and to review the literature on the association between visfatin levels and IR, cardiovascular diseases, and renal diseases in obesity.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9631142 | PMC |
http://dx.doi.org/10.12998/wjcc.v10.i30.10840 | DOI Listing |
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