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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Anabolic Steroids: Effect on Muscle, Metabolism and the Heart
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<blockquote data-quote="madman" data-source="post: 191817" data-attributes="member: 13851"><p><strong>Fig. 3 <span style="color: rgb(184, 49, 47)">Normal and AAS-influenced lipoprotein metabolism.</span> <span style="color: rgb(26, 188, 156)">During normal lipoprotein metabolism</span>, intestinally produced chylomicrons carrying dietary lipids are hydrolyzed by lipoprotein lipase<span style="color: rgb(184, 49, 47)"> (LPL)</span>. FFA are liberated and taken up by the liver, muscle, and adipose tissue. The resulting chylomicron remnants are taken up by the liver via low-density lipoprotein receptor <span style="color: rgb(184, 49, 47)">(LDL-R)</span> and the LDL receptor-related protein <span style="color: rgb(184, 49, 47)">(LRP)</span>. Meanwhile, hepatically produced VLDL transport cholesterol esters <span style="color: rgb(184, 49, 47)">(CE)</span> and TG through blood vessels, during which they undergo hydrolysis, releasing FFA which are taken up by peripheral tissues. This loss of TG means VLDL particles decrease in size <span style="color: rgb(184, 49, 47)">(and therefore density) </span>and become cholesterol-enriched and known as idLDL. Due to the action of HGTL, IDL particles become even smaller and known as LDL. LDL particles have an increased propensity to deposit cholesterol in peripheral tissues; however, they primarily transport cholesterol to the liver, where they are taken up by the LDL-R. The intestine also produces precursors which contribute towards the production of HDL. Small HDL3 particles acquire CE and TG and form larger HDL2 particles which, with the assistance of lecithin–cholesterol acyltransferase <span style="color: rgb(184, 49, 47)">(LCAT)</span>, subsequently exchange CE for even more TG with VLDL particles and chylomicrons, before traveling to the liver where they are taken up by scavenger receptor B1 <span style="color: rgb(184, 49, 47)">(SR-B1)</span> or LDL-R. <span style="color: rgb(26, 188, 156)">During AAS-influenced lipoprotein metabolism </span>HGTL is upregulated, resulting in a preponderance of more atherogenic small, dense LDL III and IV particles, as opposed to the larger and more buoyant LDL I and II particles found in normal lipoprotein metabolism. There is also a severe decrease in the number of HDL 2 and 3 particles overall, which are generally regarded as being atheroprotective </strong></p><p></p><p></p><p><span style="color: rgb(184, 49, 47)"><strong>NORMAL LIPOPROTEIN METABOLISM</strong></span></p><p>[ATTACH=full]11936[/ATTACH]</p><p></p><p><strong><span style="color: rgb(184, 49, 47)">AAS LIPOPROTEIN METABOLISM</span></strong></p><p>[ATTACH=full]11937[/ATTACH]</p></blockquote><p></p>
[QUOTE="madman, post: 191817, member: 13851"] [B]Fig. 3 [COLOR=rgb(184, 49, 47)]Normal and AAS-influenced lipoprotein metabolism.[/COLOR] [COLOR=rgb(26, 188, 156)]During normal lipoprotein metabolism[/COLOR], intestinally produced chylomicrons carrying dietary lipids are hydrolyzed by lipoprotein lipase[COLOR=rgb(184, 49, 47)] (LPL)[/COLOR]. FFA are liberated and taken up by the liver, muscle, and adipose tissue. The resulting chylomicron remnants are taken up by the liver via low-density lipoprotein receptor [COLOR=rgb(184, 49, 47)](LDL-R)[/COLOR] and the LDL receptor-related protein [COLOR=rgb(184, 49, 47)](LRP)[/COLOR]. Meanwhile, hepatically produced VLDL transport cholesterol esters [COLOR=rgb(184, 49, 47)](CE)[/COLOR] and TG through blood vessels, during which they undergo hydrolysis, releasing FFA which are taken up by peripheral tissues. This loss of TG means VLDL particles decrease in size [COLOR=rgb(184, 49, 47)](and therefore density) [/COLOR]and become cholesterol-enriched and known as idLDL. Due to the action of HGTL, IDL particles become even smaller and known as LDL. LDL particles have an increased propensity to deposit cholesterol in peripheral tissues; however, they primarily transport cholesterol to the liver, where they are taken up by the LDL-R. The intestine also produces precursors which contribute towards the production of HDL. Small HDL3 particles acquire CE and TG and form larger HDL2 particles which, with the assistance of lecithin–cholesterol acyltransferase [COLOR=rgb(184, 49, 47)](LCAT)[/COLOR], subsequently exchange CE for even more TG with VLDL particles and chylomicrons, before traveling to the liver where they are taken up by scavenger receptor B1 [COLOR=rgb(184, 49, 47)](SR-B1)[/COLOR] or LDL-R. [COLOR=rgb(26, 188, 156)]During AAS-influenced lipoprotein metabolism [/COLOR]HGTL is upregulated, resulting in a preponderance of more atherogenic small, dense LDL III and IV particles, as opposed to the larger and more buoyant LDL I and II particles found in normal lipoprotein metabolism. There is also a severe decrease in the number of HDL 2 and 3 particles overall, which are generally regarded as being atheroprotective [/B] [COLOR=rgb(184, 49, 47)][B]NORMAL LIPOPROTEIN METABOLISM[/B][/COLOR] [ATTACH type="full" alt="Screenshot (2844).png"]11936[/ATTACH] [B][COLOR=rgb(184, 49, 47)]AAS LIPOPROTEIN METABOLISM[/COLOR][/B] [ATTACH type="full" alt="Screenshot (2845).png"]11937[/ATTACH] [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Anabolic Steroids: Effect on Muscle, Metabolism and the Heart
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