High density lipoproteins, 1978 -- an overview.
High density lipoproteins (HDL) have come of age. For years it has been fashionable to study HDL as an approach to understanding lipoprotein structure and lipid binding. Available in abundant amounts from normal human plasma, readily separable into its individual lipid and soluble apolipoprotein components, HDL has provided much information for lipoprotein model building. Suddenly it has been thrust center stage clinically by a host of convincing epidemiologic studies that clearly establishes an inverse relationship between HDL levels and coronary vascular events. Biochemists, clinicians, cardiologists and epidemiologists are simultaneously focusing attention on HDL. Familial High Density Lipoprotein Deficiency (Tangier Disease) has been well described but is poorly understood as a clinical syndrome complex. We have suddenly become aware of how little we understand about HDL's normal ultracentrifugal and apoprotein heterogeneity, about its functional role(s) or the determinant(s) of its concentration in plasma. The relative contributions of the two sites of HDL origin, the liver and intestine, are yet to be determined as are the site(s) of degradation. Awareness of a problem and its importance is the first step toward the solution(s) of the problem.
D001053:Apolipoproteins / Q000097:blood; D055598:Chemical Phenomena; D002621:Chemistry; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D008075:Lipoproteins, HDL / Q000097:blood* / Q000502:physiology; D008099:Liver / Q000378:metabolism; D013631:Tangier Disease / Q000097:blood
D001053:Apolipoproteins; D008075:Lipoproteins, HDL