I had a physician argue that his diabetes patient with an HDL of 70 was safe from cardiovascular risks. He of course did know of the inner complexities of the HDL. I explained to him that in diabetes patients, a HDL may actually to proatherogenic. HDL functions by promoting cholesterol efflux and inhibiting inflammation. But, if the HDL is overloaded, such as the patient with the HDL of 70, it can actually be pro-inflammatory.
A good editorial to read....
Showing posts with label HDL. Show all posts
Showing posts with label HDL. Show all posts
Wednesday, July 8, 2009
Tuesday, February 3, 2009
HDL can be bad?
Curr Opin Lipidol. 2007 Aug;18(4):427-34.
The paradox of dysfunctional high-density lipoprotein.
Ansell BJ, Fonarow GC, Fogelman AM.
Atherosclerosis Research Unit, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA. bansell@mednet.ucla.edu
PURPOSE OF REVIEW: This review addresses how, in atherosclerosis or systemic inflammation, HDL can lose its usual atheroprotective characteristics and even paradoxically assume proinflammatory properties.
RECENT FINDINGS: Specific chemical and structural changes within HDL particles can impede reverse cholesterol transport, enhance oxidation of LDL, and increase vascular inflammation. HDL may be viewed as a shuttle that can be either anti-inflammatory or proinflammatory, depending on its cargo of proteins, enzymes, and lipids. Some therapeutic approaches that reduce coronary risk, such as statins and therapeutic lifestyle changes, can favorably moderate the characteristics of proinflammatory HDL. In addition, apolipoprotein A-I mimetic peptides and other compounds that target functional aspects of HDL may offer novel approaches to reduction in cardiovascular risk.
SUMMARY: Current data suggest that under some conditions HDL can become dysfunctional and even proinflammatory, but this characterization can change with resolution of systemic inflammation or use of certain treatments.
The paradox of dysfunctional high-density lipoprotein.
Ansell BJ, Fonarow GC, Fogelman AM.
Atherosclerosis Research Unit, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA. bansell@mednet.ucla.edu
PURPOSE OF REVIEW: This review addresses how, in atherosclerosis or systemic inflammation, HDL can lose its usual atheroprotective characteristics and even paradoxically assume proinflammatory properties.
RECENT FINDINGS: Specific chemical and structural changes within HDL particles can impede reverse cholesterol transport, enhance oxidation of LDL, and increase vascular inflammation. HDL may be viewed as a shuttle that can be either anti-inflammatory or proinflammatory, depending on its cargo of proteins, enzymes, and lipids. Some therapeutic approaches that reduce coronary risk, such as statins and therapeutic lifestyle changes, can favorably moderate the characteristics of proinflammatory HDL. In addition, apolipoprotein A-I mimetic peptides and other compounds that target functional aspects of HDL may offer novel approaches to reduction in cardiovascular risk.
SUMMARY: Current data suggest that under some conditions HDL can become dysfunctional and even proinflammatory, but this characterization can change with resolution of systemic inflammation or use of certain treatments.
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