Untitled Page

April 21, 2006

Regulation of Lecithin:Cholesterol Acyltransferase (LCAT) and Cholesteryl Ester Transfer Protein (CETP) by Dietary Jojoba Oil and/or Cholesterol in New Zealand White Rabbits
Presenter: Maritza Hernandez
Advisor: Dr. Raymond E. Garcia
Abstract:  Cardiovascular disease (CVD) is the leading cause of death in the United States, primarily due to elevated serum cholesterol concentrations.  The objective of this research is to determine why previous dietary studies indicate high density lipoprotein cholesterol concentr! ation [HDL-C] decreases in cholesterol-fed rabbits and is maintained at a normal concentration in cholesterol + jojoba oil- fed rabbits.  It is our hypothesis that dietary jojoba oil in the presence or absence of dietary cholesterol activates lecithin:cholesterol acyltransferase (LCAT)  and inhibits cholesteryl ester transfer protein (CETP).  This hypothesis was tested by feeding New Zealand White rabbits a normal (N), 3% jojoba oil (J), 1% cholesterol (C), or 1% cholesterol+3% jojoba oil (CJ) diet for seven days.  Blood samples were collected before the start of the experimental diets (day 0) and seven days after the initiation of the diets (day 7).  Total cholesterol (TC) and free cholesterol (FC) concentrations were measured enzymatically, the rate of CETP was ! obtained with a fluorometric assay, and the rate of LCAT was found by measuring the loss of FC over a three hour time frame.  Rabbits showed greater [HDL-CE] in the J-fed and CJ-fed rabbits compared to the N-fed and J-fed rabbits respectively.  Rabbits fed the CJ diet exhibit an increase in [HDL-FC] and a reduction in [HDL-CE], keeping [HDL-C] at a normal level.  LCAT activity was greater in the C- and CJ-fed rabbits than it was for the N- and J- fed rabbits.  CETP activity was lower in CJ-fed rabbits than in C-fed rabbits, but both had a greater CETP activity than the N- and J-fed rabbits.  These results suggest dietary jojoba oil inhibits CETP and activates LCAT in the presence of dietary cholesterol. (Supported by NIH-MBRS-RISE grant R25 GM61331 and NIH-MARC grant! T34 GM 08228.)