Bethesda, Md. -- Scientists have shown for the first time that a protein involved in the transfer of fat in the blood may also influence how fat cells store fat. Richard E. Morton and Lahoucine Izem, research scientists at the Cleveland Clinic Foundation, have shown that the protein, called cholesteryl ester transfer protein (CETP), is involved in the cellular storage and regulation of cholesterol and other fats and, as a result, probably has unexpected contributions to obesity and diabetes.
CETP is known to shuttle different types of fat between lipoproteins combinations of fat and protein that transport fats in the blood, Morton says. In this study, we show that CETP also shuttles fats inside fat cells between two separate areas and that fat cells with reduced levels of CETP are unable to process fats normally.
The new study, to be published in the July 27 issue of the Journal of Biological Chemistry, was selected as a Paper of the Week by the journals editors, meaning that it belongs to the top one percent of papers reviewed in significance and overall importance.
Research performed during the past decade has shown that CETP affects how a type of fat called cholesteryl ester is moved from the blood plasma into cells. Since fat cells make abundant CETP, Morton and Izem decided to examine what CETP does inside a fat cell and what would happen to fat cells that are deficient in CETP.
The scientists noticed that fat cells lacking CETP could not make and store cholesterol, cholesteryl ester, and another fat called triglyceride like normal fat cells do. In CETP-deficient cells, cholesteryl ester and triglyceride accumulated in a cellular compartment called the endoplasmic reticulum (ER), while an abnormally low amount of these fats was seen in lipid droplets local accumulations of fat in fat cells.
Morton and Izem suggest that, in normal cells, CETP transfers cholesteryl ester an
Contact: Pat Pages
American Society for Biochemistry and Molecular Biology