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	<title>Translations:Niacin/34/en - Revision history</title>
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	<updated>2026-05-19T12:04:23Z</updated>
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		<title>FuzzyBot: Importing a new version from external source</title>
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		<updated>2024-02-20T00:42:51Z</updated>

		<summary type="html">&lt;p&gt;Importing a new version from external source&lt;/p&gt;
&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;===Mechanisms===&lt;br /&gt;
Niacin reduces synthesis of low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), [[lipoprotein(a)]] and [[triglycerides]], and increases [[high-density lipoprotein]] cholesterol (HDL-C). The lipid-therapeutic effects of niacin are partly mediated through the activation of [[G protein-coupled receptor]]s, including [[hydroxycarboxylic acid receptor 2]] (HCA&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;)and [[hydroxycarboxylic acid receptor 3]] (HCA&amp;lt;sub&amp;gt;3&amp;lt;/sub&amp;gt;), which are highly expressed in [[adipose tissue|body fat]]. HCA&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; and HCA&amp;lt;sub&amp;gt;3&amp;lt;/sub&amp;gt; inhibit [[cyclic adenosine monophosphate]] (cAMP) production and thus suppress the release of free [[fatty acids]] (FFAs) from body fat, reducing their availability to the liver to synthesize the blood-circulating lipids in question. A decrease in free fatty acids also suppresses liver expression of [[apolipoprotein C3]] and [[PPARGC1B|PPARg coactivator-1b]], thus increasing VLDL-C turnover and reducing its production. Niacin also directly inhibits the action of [[diacylglycerol O-acyltransferase 2]] (DGAT2) a key enzyme for triglyceride synthesis.&lt;/div&gt;</summary>
		<author><name>FuzzyBot</name></author>
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