Nice animated overview of phospholipid structure and how these fats are important to cell membranes:
Here we have assembled some papers and thoughts that examine the structure of lipoproteins:
Wu et al. 2007. The refined structure of nascent HDL reveals a key functional domain for particle maturation and dysfunction. Nature Structural & Molecular Biology. 14: 861-868.
Segrest JP et al. 2001. Structure of apoliprotein B-100 in LDL. Journal of Lipid Research. 42: 1346-1367.
Jeon H & Blacklow SC. 2005. Structure and physiological function of the LDLr. Annual Review of Biochemistry. 74: 535-562.
Can be produced directly 1
Small VLDL2 / large IDL1 lead to mid sized LDL2, while small IDL2which is similar in size and density to large LDL1, is the metabolic precursor to these particles. IDL1 is part of a delipidation cascade, thus we go VLDL->IDL -> LDL, but IDL2 is directly secreted (possibly in the liver), and thus the arising LDL remains in the same size and density region.
1Gaw, A., C. J. Packard, G. M. Lindsay, B. A. Griffin, M. J. Caslake, A. R. Lorimer, and J. Shepherd. 1995. Overproduction of small very low density lipoproteins (Sf 20–60) in moderate hypercholesterolemia: relationships between apolipoprotein B kinetics and plasma lipoproteins. J. Lipid Res. 36: 158–171.
Secreted throughout the VLDL-LDL-IDL spectrum 1,2,3. Inversely related to TGs4, such that at low TG ApoB is released as IDL / LDL but at high TG 90% of ApoB is secreted in VLDL
1Fisher, W. R., L. A. Zech, L. L. Kilgore, and P. W. Stacpoole. 1991.Metabolic pathways of apolipoprotein B in heterozygous familial hypercholesterolemia: studies with a [3H]leucine tracer. J. Lipid Res. 32: 1823–1836.
2Soutar, A. K., N. B. Myant, and G. R. Thompson. 1977. Simultaneous measurement of apolipoprotein B turnover in very-lowand low-density lipoproteins in familial hypercholesterolaemia. Atherosclerosis. 28: 247–256.
3Nakaya, N., B. H. Chung, J. R. Patsch, and O. D. Taunton. 1977. Synthesis and release of low density lipoproteins by the isolated perfused pig liver. J. Biol. Chem. 252: 7530–7533.
4Packard, C. J., T. Demant, J. P. Stewart, D. Bedford, M. J. Caslake, G. Schwertfeger, A. Bedynek, J. Shepherd, and D. Seidel. 2000. Apolipoprotein B metabolism and the distribution of VLDL and LDL subfractions. J. Lipid Res. 41: 305–318.
Variation in plasma TG mainly varies with levels of VLDL1 levels 1. This variation affects how ApoB is secreted – at low TG, ApoB is secreted as IDL or LDL, at high levels of TG it is secreted as VLDL.
High TG should lead to increased VLDL, and increased LDL from delipidation cascades, it should reduce the amount of directly synthesized LDL. LDL that is directly synthesized is larger than that which is a VLDL remnant, therefore reducing TG levels, should lead to an increased in the overall size of LDL.
1Gofman, J. W., O. Delalla, F. Glazier, N. K. Freeman, D. Lindgren, A. V. Nichols, B. Strisower, and A. R. Tramplin. 1954. The serum lipoprotein transport system in health, metabolic disorders, atherosclerosis and coronary artery disease. Plasma. 2: 413–484.
Interacts with (to inhibit) or displaces ApoE1,2,3,4
1Aalto-Setala, K., E. A. Fisher, X. Chen, T. Chajek-Shaul, T. Hayek, R. Zechner, A. Walsh, R. Ramakrishnan, H. N. Ginsberg, and J. L. Breslow. 1992. Mechanism of hypertriglyceridemia in human apolipoprotein (apo) CIII transgenic mice. Diminished very low density lipoprotein fractional catabolic rate associated with increased apoCIII and reduced apoE on the particles. J. Clin. Invest. 90: 1889–1900.
2Windler, E., Y. Chao, and R. J. Havel. 1980. Regulation of the hepatic uptake of triglyceride-rich lipoproteins in the rat. Opposing effects of homologous apolipoprotein E and individual C apolipoproteins. J. Biol. Chem. 255: 8303–8307.
3Windler, E., Y. Chao, and R. J. Havel. 1980. Determinants of hepatic uptake of triglyceride-rich lipoproteins and their remnants in the rat. J. Biol. Chem. 255: 5475–5480.
4Windler, E., and R. J. Havel. 1985. Inhibitory effects of C apolipoproteins from rats and humans on the uptake of triglyceride-rich lipoproteins and their remnants by the perfused rat liver. J. Lipid Res. 26: 556–565.
This blog-iki (blog because I don’t know how to make a wiki properly) is not intended to be original, citeable material. Rather just an online resource for collected notes on lipid reading I / we have conducted. Therefore below is a list of papers that have largely contributed to the knowledge herein:
Berneis KK, Krauss RM. Metabolic origins and clinical significance of LDL heterogeneity. J Lipid Res 2002;43:1363-79: Great article on the origin of small, dense LDLs