New links were found between obesity and cardiovascular disease when researchers applied novel methods to detect binding of fatty acids to CD36 and their effect on internalization of oxidized LDL.
The study was led by James A. Hamilton, PhD, professor of Physiology, Biophysics and Radiology at Boston University School of Medicine.
Although other research groups have characterized a fatty acid binding site on CD36 and postulated CD36 to be a gatekeeper for fatty acid entry into cells, the Hamilton lab previously found that CD36 did not increase fatty acid translocation across the plasma membrane.
In the current study all of the common dietary fatty acid types (saturated, unsaturated, trans and polyunsaturated) were shown by a new assay to bind to CD36 at levels greater than expected for a single binding site characterized in previous studies.
In cells with CD36 present in the plasma membrane, all of the fatty acids also enhanced oxidized LDL uptake, except for the fish oil fatty acid DHA. This current study added to the possible mechanisms for fish oil benefits that are now widely recognized.
Hamilton said that since obesity and type 2 diabetes are characterized by high plasma levels of fatty acids, the demonstrated enhancement of oxLDL uptake by increases in common dietary fatty acids might contribute to the pathophysiology of these diseases.
The new results provided a link between fatty acids, CD36, and atherosclerosis and new drugs could be designed that target the exact mechanism more precisely, he further added.
The study is published in the Journal of Biological Chemistry.