Using a novel small-angle X-ray scattering (SAXS) method for determination of fractional and subfractional composition of lipoproteins (LPs), a significant elevation of total cholesterol-lipop- roteins (C-LP) and, esp...Using a novel small-angle X-ray scattering (SAXS) method for determination of fractional and subfractional composition of lipoproteins (LPs), a significant elevation of total cholesterol-lipop- roteins (C-LP) and, especially, total triglyceride- lipoproteins (TG-LP), was shown in this work. Among the LP fractions, poloxamer 407 was shown to significantly increase proatherogenic total C-LDL, TG-LDL and, especially, their precursors C-VLDL and TG-VLDL, while only exhibiting a moderate increase in the antiatherogenic C-HDL and TG-HDL fractions. With regard to the VLDL subfractions, significant elevations were observed in both subfractions studied;namely, C-VLDL1-2 and C-VLDL3-5. Similar chang- es were noted in the TG-VLDL1-2 and TG- VLDL3-5 subfractions. The C-IDL and TG-IDL subfractions were increased significantly (?20- to 30- fold), while the C-LDL1-3 subfraction was moderately (?3- to 5-fold) increased at 48 hrs and at day 4. In the moderately elevated (?2- to 4-fold) anti-atherogenic HDL fraction, the C-HDL2 subfraction was increased more significantly (?4- fold) compared to the C-HDL3 subfraction;how- ever, both C-HDL subfractions returned to base- line by day 4. The elevation in the TG-HDL2 subfraction was observed only at 24 hrs. Mouse models of hyperlipidemia and atherosclerosis are useful to evaluate the role of “individual” LPs, as well as their fractions and subfractions, in hyperlipidemia and the genesis of atherosclerosis.展开更多
文摘Using a novel small-angle X-ray scattering (SAXS) method for determination of fractional and subfractional composition of lipoproteins (LPs), a significant elevation of total cholesterol-lipop- roteins (C-LP) and, especially, total triglyceride- lipoproteins (TG-LP), was shown in this work. Among the LP fractions, poloxamer 407 was shown to significantly increase proatherogenic total C-LDL, TG-LDL and, especially, their precursors C-VLDL and TG-VLDL, while only exhibiting a moderate increase in the antiatherogenic C-HDL and TG-HDL fractions. With regard to the VLDL subfractions, significant elevations were observed in both subfractions studied;namely, C-VLDL1-2 and C-VLDL3-5. Similar chang- es were noted in the TG-VLDL1-2 and TG- VLDL3-5 subfractions. The C-IDL and TG-IDL subfractions were increased significantly (?20- to 30- fold), while the C-LDL1-3 subfraction was moderately (?3- to 5-fold) increased at 48 hrs and at day 4. In the moderately elevated (?2- to 4-fold) anti-atherogenic HDL fraction, the C-HDL2 subfraction was increased more significantly (?4- fold) compared to the C-HDL3 subfraction;how- ever, both C-HDL subfractions returned to base- line by day 4. The elevation in the TG-HDL2 subfraction was observed only at 24 hrs. Mouse models of hyperlipidemia and atherosclerosis are useful to evaluate the role of “individual” LPs, as well as their fractions and subfractions, in hyperlipidemia and the genesis of atherosclerosis.
