In trauma and infection the PCSK9 (inhibitor for LDL receptor) is increased. Therefore we expect increase in plasma LDL level, nevertheless there is reduction in LDL level.
Hello,
as you know, LDL is produced by liver. You just mention LDL receptors, however, it is necessary to consider LDL production. Also, there are evidences showing cholesterol and HDL fall during infection. It may be related to the activity of LPL. The following article may be useful:
http://www.sciencedirect.com/science/article/pii/0026049588901205
As we know that injuries or trauma may be associated with hyperglycemia as a transient state , hormones and other mediators are contributing to this . ACTH , cortisol are major factors her , additionally they represent a cholesterol bioproducts.
It seems likely or our suggestion her that shift of cholesterol pathway to provide these chlesterol biproducts may contribute to such hypocholesterolemic state
Interesting question.
Cholesterol is certainly used to produce corticosteroids, as suggested above, but I believe that HDL cholesterol is the main source.
Maybe the release of acute phase proteins during trauma that interfere with cholesterol metabolism, such as serum amyloid a, has something to do with it. But then again, SAA affects mainly HDL metabolism. Does anyone know if SAA blocks PCSK9?
Or the drop is perhaps due to oxidation of LDL during trauma, which is then cleared by macrophages?
I think we have many explanation:
Blocking of PCSK9 by SAA
Clearance of ox. LDL by macrophages
Shifting of cholesterol to provide cholesterol bi-products. but this factor unlikely as the level of PCSK9 is high which will reduce the LDL receptor.