Lamellar Lipoproteins Uniquely Contribute to Hyperlipidemia in Mice Doubly Deficient in Apolipoprotein E and Hepatic Lipase

摘要: Remnants of triglyceride-rich lipoproteins containing apolipoprotein (apo) B-48 accumulate in apo E-deficient mice, causing pronounced hypercholesterolemia. Mice doubly deficient E and hepatic lipase have more hypercholesterolemia, even though remnants do not appreciably mice alone. Here we show that the manifest a unique lamellar hyperlipoproteinemia, characterized by vesicular particles 600 Å–1,300 Å diameter. As seen negative-staining electron microscopy, these also contain an electron-lucent region adjacent to vesicle wall, similar core typical lipoproteins. Correlative chemical analysis indicates wall is composed 1:1 molar mixture cholesterol phospholipids, whereas appears be cholesteryl esters (about 12% particle mass). Like spherical B-48, but they are particularly rich A-IV. We propose removed from scavenger receptor B1, leaving behind polar lipid-rich fuse form Hepatic may prevent such accumulating hydrolyzing phosphatidyl choline as B1 removes gradual endocytosis bound on surface hepatocytes.