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| __NOTOC__
| | #Redirect [[High density lipoprotein physiology]] |
| {{High density lipoprotein}}
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| {{CMG}}; {{AE}} {{AN}}; {{RT}}
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| ==Pathophysiology==
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| ===Structure and Function===
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| HDL are the smallest of the lipoproteins. They are the densest because they contain the highest proportion of [[protein]]. They contain the A class of [[apolipoprotein]]s. The liver synthesizes these lipoproteins as complexes of apolipoproteins and phospholipid, which resemble cholesterol-free flattened spherical lipoprotein particles. They are capable of picking up cholesterol, carried internally, from cells they interact with. A [[Blood plasma|plasma]] enzyme called [[lecithin-cholesterol acyltransferase]] (LCAT) converts the free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol) which is then sequestered into the core of the lipoprotein particle eventually making the newly synthesized HDL spherical. They increase in size as they circulate through the bloodstream and incorporate more cholesterol molecules into their structure. Thus it is the concentration of large HDL particles which more accurately reflects protective action, as opposed to the concentration of total HDL particles.<ref>Kwiterovich PO. The Metabolic Pathways of High-Density Lipoprotein, Low-Density Lipoprotein, and Triglycerides: A Current Review. Am J Cardiol 2000;86(suppl):5L.</ref> This ratio of large HDL to total HDL particles varies widely and is only measured by more sophisticated lipoprotein assays using either [[electrophoresis]] (the original method developed in the 1970s), or newer [[Nuclear magnetic resonance|NMR]] spectroscopy, [[NMR spectroscopy]] methods, developed in the 1990s.
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| HDL particles are not inherently protective. It is only the HDL particles which become the largest (actually picking up and carrying cholesterol) which are protective. There is no reliable relationship between total HDL and large HDL, and more sophisticated analyses which actually measure large HDL, not just total, correlate much better with clinical outcomes.
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| In the [[fight-or-flight response|stress response]], [[serum amyloid A]], which is one of the [[acute phase proteins]] and an apolipoprotein, is under the stimulation of [[cytokine]]s ([[Interleukin 1|IL-1]], [[Interleukin 6|IL-6]]) and [[cortisol]] produced in the [[adrenal cortex]] and carried to the damaged tissue incorporated into HDL particles. At the inflammation site, it attracts and activates leukocytes. In chronic inflammations, its deposition in the tissues manifests itself as [[amyloidosis]].
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| Men tend to have noticeably lower HDL levels, with smaller size and lower cholesterol content, than women. Men also have an increased incidence of [[atherosclerosis|atherosclerotic]] heart disease.
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| Historically, beginning in the late 1970's cholesterol and lipid assays were promoted to estimate total HDL-cholesterol because such tests used to be far less expensive, by about 50 fold, than measured lipoprotein particle concentrations and subclass analysis. Over time, with continued research, decreasing costs, greater availability and wider acceptance of other "lipoprotein subclass analysis" assay methods, including [[NMR spectroscopy]], human studies have continued to show a stronger correlation between human clinically obvious cardiovascular events and quantitatively measured large HDL-particle concentrations.
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| ==References==
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| {{Reflist|2}}
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| [[Category:Lipid disorders]]
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| [[Category:Cardiology]]
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| [[Category:Lipoproteins]]
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