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<pubDate>Thu, 21 Aug 2008 04:53:17 BST</pubDate>


	<title>CiteULike: omalbams Chansky</title>
	<description>CiteULike: omalbams Chansky</description>


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    <title>Testosterone administration to men increases hepatic lipase activity and decreases HDL and LDL size in 3 wk</title>
    <link>http://www.citeulike.org/user/omalbam/article/2323185</link>
    <description>&lt;i&gt;Am J Physiol Endocrinol Metab, Vol. 284, No. 6. (1 June 2003), pp. E1112-1118.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Testosterone administration to men is known to decrease high-density lipoprotein cholesterol (HDL-C) and the subclasses HDL2 and HDL3. It also might increase the number of small, dense, low-density lipoprotein cholesterol (LDL-C) particles in hypogonadal men. The decrease in HDL-C and in LDL-C size is potentially mediated by hepatic lipase activity, which hydrolyzes lipoprotein phospholipids and triacylglycerol. To determine how HDL-C and LDL-C particles are affected by testosterone administration to eugonadal men, testosterone was administered as a supraphysiological dose (600 mg/wk) for 3 wk to elderly, obese, eugonadal men before elective hip or knee surgery, and lipids were measured by routine methods and by density gradient ultracentrifugation. Hepatic lipase activity increased &#62;60% above baseline levels, and HDL-C, HDL2, and HDL3 significantly declined in 3 wk. In addition, the LDL-C peak particle density and the amount of LDL-C significantly increased. Testosterone is therefore a potent stimulator of hepatic lipase activity, decreasing HDL-C, HDL2, and HDL3 as well as increasing LDL particle density changes, all associated with increased cardiovascular risk. 10.1152/ajpendo.00524.2002</description>
    <dc:title>Testosterone administration to men increases hepatic lipase activity and decreases HDL and LDL size in 3 wk</dc:title>

    <dc:creator>Karen Herbst</dc:creator>
    <dc:creator>John Amory</dc:creator>
    <dc:creator>John Brunzell</dc:creator>
    <dc:creator>Howard Chansky</dc:creator>
    <dc:creator>William Bremner</dc:creator>
    <dc:identifier>doi:10.1152/ajpendo.00524.2002</dc:identifier>
    <dc:source>Am J Physiol Endocrinol Metab, Vol. 284, No. 6. (1 June 2003), pp. E1112-1118.</dc:source>
    <dc:date>2008-02-02T15:11:24-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Am J Physiol Endocrinol Metab</prism:publicationName>
    <prism:volume>284</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>E1112</prism:startingPage>
    <prism:endingPage>1118</prism:endingPage>
    <prism:category>aging</prism:category>
    <prism:category>hplp</prism:category>
    <prism:category>physiology</prism:category>
    <prism:category>rct</prism:category>
    <prism:category>testosterone</prism:category>
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