https://wiki.tiffa.net/w/index.php?action=history&feed=atom&title=Translations%3AMetabolic_syndrome%2F23%2FenTranslations:Metabolic syndrome/23/en - Revision history2026-09-08T18:41:11ZRevision history for this page on the wikiMediaWiki 1.43.0https://wiki.tiffa.net/w/index.php?title=Translations:Metabolic_syndrome/23/en&diff=122556&oldid=prevFuzzyBot: Importing a new version from external source2024-02-28T01:37:50Z<p>Importing a new version from external source</p>
<p><b>New page</b></p><div>==Pathophysiology==<br />
It is common for there to be a development of [[visceral fat]], after which the [[adipocyte]]s (fat cells) of the visceral fat increase [[blood plasma|plasma]] levels of [[TNF-α]] and alter levels of other substances (e.g., [[adiponectin]], [[resistin]], and [[PAI-1]]). TNF-α has been shown to cause the production of inflammatory [[cytokine]]s and also possibly trigger cell signaling by interaction with a [[TNF receptor superfamily|TNF-α receptor]] that may lead to insulin resistance. An experiment with rats fed a diet with 33% [[sucrose]] has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. The progression from visceral fat to increased TNF-α to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.</div>FuzzyBot