Deneys van der Westhuyzen, Ph.D.
Professor
541 CT Wethington Bldg.
900 South Limestone
Lexington, KY 40536-0200
Tel: (859)-323-4933 ext 81397
Fax: (859)-257-3646
e-mail: dvwest1@uky.edu
Publication Listing on PubMed
Academic Appointments:
• Departments of Internal Medicine, Molecular, and Cellular Biochemistry
• Graduate Center for Nutritional Sciences
Education:
• B.Sc.(Hons), Biochemistry, University of the Witwatersrand Johannesburg,
South Africa
• Ph.D. (Biochemistry), University of Cape Town, South Africa
• Postdoctoral, State University of New York, Downstate Medical
Awards:
• USPHS Fogarty Postdoctoral Research Fellow
• Fellow of the University of Cape Town
• Fellow of the Royal Society of South Africa
Specific Interests in nutrition:
Lipoprotein receptors, and their role in lipoprotein metabolism and atherosclerosis.
Research:
Research in Dr. van der Westhuyzen’s laboratory is focused on lipoprotein receptors and how such receptors contribute to or protect against artherosclerosis. Oxidized and modified lipoproteins play a key role in the development of atherosclerosis and his laboratory is studying various scavenger receptors that mediate the metabolism of such lipoprotein particles. The effect of dietary cholesterol and high fat “Western Diet” on the expression of scavenger receptors is being studied. One such receptor, the scavenger receptor-BI (SR-BI), is also a newly described receptor for HDL. SR-BI mediates the selective delivery of HDL Cholesterol cells and is a candidate receptor for mediating “reverse cholesterol transport” from extrahepatic tissues to the liver. He has shown that SR-BI exists as alternate-spliced variants and is currently studying the significance and biological functions of these isoforms. This includes an investigation of the regulation of expression of SR-BI isoforms in different tissues and the regulation by cholesterol and oxidized lipids. A central hypothosis being examined is that modification of HDL during inflammation leads to alterations of metabolic changes including a major modulation of HDL structure. Such changes would have important implications for HDL metabolism and could affect HDL-mediated cholesterol delivery to the liver, as well as cholesterol flux between HDL and cells in localized atherosclerotic lesions.
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