Dietary supplementation with concentrated RGJ improves the lipoprotein profile, reduces plasma concentrations of inflammatory biomarkers and oxidized LDL, and may favor a reduction in cardiovascular disease risk.

Lipoprotein metabolism is regulated by the functional interplay between lipoprotein components and the receptors and enzymes with which they interact. Recent evidence indicates that the structurally related glycoproteins CD36 and SR-BI act as cell surface receptors for some lipoproteins. Thus, CD36 has been reported to bind oxidized LDL (OxLDL) and acetylated LDL (AcLDL), while SR-BI also binds native LDL and HDL. The cDNA of human CLA-1 predicts a protein 509 amino acids long that displays a 30% and an 80% amino acid identity with CD36 and mouse or hamster SR-BI, respectively. In this report, we describe the structural characterization of CLA-1 as an 85-kD plasma membrane protein enriched in N-linked carbohydrates. The expression of CLA-1 on mammalian and insect cells has been used to demonstrate that CLA-1 is a high-affinity specific receptor for the lipoproteins HDL, LDL, VLDL, OxLDL, and AcLDL. Northern blot analysis of the tissue distribution of CLA-1 in humans indicated that its expression is mostly restricted to tissues performing very active cholesterol metabolism (liver and steroidogenic tissues). This finding, in the context of the capability of this receptor to bind to both native and modified lipoproteins, strongly suggests that the CLA-1 receptor contributes to lipid metabolism and atherogenesis.

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On the basis of bibliographic references and new own data, major adaptations of lipid metabolism occurring at late gestation are reviewed. Maternal hypertriglyceridemia at late gestation results from the juxtaposition of several factors: (1) enhanced adipose tissue lipolysis facilitating the availability to the liver of substrates for triglyceride synthesis and contributing to augmented flux of very low density lipoproteins (VLDL) into the circulation; (2) maternal hyperphagia and unmodified gut lipid absorption increasing chylomicron formation from dietary lipid; (3) reduced lipoprotein lipase (LPL) activity in extrahepatic tissues (especially adipose tissue) which does not allow a triglyceride removal proportional to their enhanced production. It is proposed that these changes are also responsible for the altered composition of VLDL in late pregnancy. In conditions of food deprivation the use of glycerol released from adipose tissue as preferential gluconeogenic substrate, and the enhanced maternal ketogenesis warrants the availability of fuels for the fetus. Just prior to parturition the increase in mammary gland LPL activity is responsible for the reduction in circulating triglycerides and prepares the mother for lactation.

Mouse and hamster SR-BI glycoproteins and their putative human counterpart CLA-I are so far the only scavenger receptors known to bind both native and modified lipoproteins. CD36, a multigland glycoprotein structurally related to SR-BI and CLA-1, has been reported to bind oxidized low density lipoprotein (OxLDL) and acetylated LDL (AcLDL). In this report, we have studied the ability of CD36 to bind native lipoproteins. By transient expression of human CD36 in mammalian and insect cells, we demonstrate that CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, VLDL, and, as previously reported, for OxLDL and AcLDL. The specificity of these interactions is supported by the dosedependent inhibitory effect of a monoclonal antibody against CD36. Furthermore, at least for HDL, binding to CD36 does not require the presence of apoE. These findings, together with preferential expression of CD36 in tissues performing very active fatty acid metabolism (skeletal muscle, heart, mammary epithelium, and adipose tissue) and its involvement in foam cell formation (macrophages), suggest that binding of lipoproteins to CD36 might contribute to the regulation of lipid metabolism, and to the pathogenesis of atherosclerosis. -