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Frederick C. de Beer, M.D.
FCDEBE1's picture
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fcdebe1@uky.edu
859-323-5079
900 S. Limestone Street
Imflammation and Lipoprotein Metabolism Research Group
Position(s): 
Dean/Vice Pres Clinical Academic Affairs
Affiliation(s): 
Cardiovascular Research Center
Other Affiliation(s): 
MD/PhD Program Mentor
CVRC - Core Faculty
Inflammation and Lipoprotein Metabolism Research Group
Microbiology, Immunology & Molecular Genetics - Adjunct Faculty
Nutritional Sciences Graduate Faculty
Pharmacology and Nutritional Sciences - Joint Faculty
Research Description: 

Our group investigates the impact of inflammation and insulin resistance on lipoprotein and cellular metabolism. In one project, we are investigating how inflammation and insulin resistance alters the metabolism and function of high-density lipoprotein (HDL). For decades, HDL has been considered to be the “good cholesterol” because individuals with high levels of HDL in their blood are at lower risk for cardiovascular disease (heart attack and stroke) compared to individuals with low HDL. HDL is thought to protect against cardiovascular disease through its ability to transport “bad” cholesterol that has accumulated in blood vessels back to the liver, where it can be removed from the body. Our group investigates the hypothesis that inflammation and insulin resistance interferes with HDL’s ability to carry out this protective function. Many of our studies focus on serum amyloid A (SAA). SAA is an acute phase reactant whose secretion by the liver can increase up to 1000-fold during severe inflammation, such as sepsis. Virtually all of the SAA in the blood is associated with HDL. We are investigating whether persistent elevations of SAA in individuals with chronic inflammation or insulin resistance leads to detrimental effects in blood vessels and other tissues. We also study secretory phospholipase A2 (sPLA2’s), a class of secreted enzymes that can hydrolyze phospholipids on cell membranes and lipoprotein particles. We have determined that their activity is increased during inflammation and are currently studying how these enzymes impact cell metabolism.

PubMed Publications: 
  • Ji, A.; Wang, X.; Noffsinger, VP ; Jennings, D ; De Beer, MC ; Beer, FC ; Tannock, LR ; Webb, NR "Serum amyloid A is not incorporated into HDL during HDL biogenesis." Journal of lipid research 61, 3 (2020): 328-337. [PubMed Link] | [ Full text ]
  • Lee, JW ; Stone, ML ; Porrett, PM ; Thomas, SK ; Komar, CA ; Li, JH ; Delman, D ; Graham, K ; Gladney, WL ; Hua, X.; Black, TA ; Chien, AL ; Majmundar, KS ; Thompson, JC ; Yee, SS ; O'Hara, MH ; Aggarwal, C ; Xin, D.; Shaked, A.; Gao, M.; Liu, D.; Borad, MJ ; Ramanathan, RK ; Carpenter, EL ; Ji, A.; De Beer, MC ; Beer, FC ; Webb, NR ; Beatty, GL "Hepatocytes direct the formation of a pro-metastatic niche in the liver." Nature 567, 7747 (2019): 249-252. [PubMed Link] | [ Full text ]
  • Thompson, JC ; Wilson, PG ; Shridas, P.; Ji, A.; Beer, M.; Beer, FC ; Webb, NR ; Tannock, LR "Serum amyloid A3 is pro-atherogenic." Atherosclerosis 268, (2018): 32-35. [PubMed Link] | [ Full text ]
  • Tannock, LR ; De Beer, MC ; Ji, A.; Shridas, P.; Noffsinger, VP ; Hartigh, L.; Chait, A.; Beer, FC ; Webb, NR "Serum amyloid A3 is a high density lipoprotein-associated acute-phase protein." Journal of lipid research 59, 2 (2018): 339-347. [PubMed Link] | [ Full text ]
  • Wilson, PG ; Thompson, JC ; Shridas, P.; McNamara, PJ ; De Beer, MC ; Beer, FC ; Webb, NR ; Tannock, LR "Serum Amyloid A Is an Exchangeable Apolipoprotein." Arteriosclerosis, thrombosis, and vascular biology 38, 8 (2018): 1890-1900. [PubMed Link] | [ Full text ]
  • Kim, MH ; De Beer, MC ; Wroblewski, JM ; Charnigo, RJ ; Ji, A.; Webb, NR ; Beer, FC ; Westhuyzen, DR "Impact of individual acute phase serum amyloid A isoforms on HDL metabolism in mice." Journal of lipid research 57, 6 (2016): 969-79. [PubMed Link] | [ Full text ]
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