Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin

Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoprotei...
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Autor*in:	Nuntakorn Thongtang [verfasserIn] Margaret R. Diffenderfer [verfasserIn] Esther M.M. Ooi [verfasserIn] P. Hugh R. Barrett [verfasserIn] Scott M. Turner [verfasserIn] Ngoc-Anh Le [verfasserIn] W. Virgil Brown [verfasserIn] Ernst J. Schaefer [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	lipoproteins/kinetics LDL subfractions statins dyslipidemia atherosclerosis mass spectrometry

Übergeordnetes Werk:	In: Journal of Lipid Research - Elsevier, 2021, 58(2017), 7, Seite 1315-1324
Übergeordnetes Werk:	volume:58 ; year:2017 ; number:7 ; pages:1315-1324

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1194/jlr.M073882

Katalog-ID:	DOAJ055719996

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520			\|a Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL.
650		4	\|a lipoproteins/kinetics
650		4	\|a LDL subfractions
650		4	\|a statins
650		4	\|a dyslipidemia
650		4	\|a atherosclerosis
650		4	\|a mass spectrometry
653		0	\|a Biochemistry
700	0		\|a Margaret R. Diffenderfer \|e verfasserin \|4 aut
700	0		\|a Esther M.M. Ooi \|e verfasserin \|4 aut
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spelling	10.1194/jlr.M073882 doi (DE-627)DOAJ055719996 (DE-599)DOAJbbaf1b6f3bb64fa0936b86dcc2d2e91c DE-627 ger DE-627 rakwb eng QD415-436 Nuntakorn Thongtang verfasserin aut Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL. lipoproteins/kinetics LDL subfractions statins dyslipidemia atherosclerosis mass spectrometry Biochemistry Margaret R. Diffenderfer verfasserin aut Esther M.M. Ooi verfasserin aut P. Hugh R. Barrett verfasserin aut Scott M. Turner verfasserin aut Ngoc-Anh Le verfasserin aut W. Virgil Brown verfasserin aut Ernst J. Schaefer verfasserin aut In Journal of Lipid Research Elsevier, 2021 58(2017), 7, Seite 1315-1324 (DE-627)26601593X (DE-600)1466675-3 15397262 nnns volume:58 year:2017 number:7 pages:1315-1324 https://doi.org/10.1194/jlr.M073882 kostenfrei https://doaj.org/article/bbaf1b6f3bb64fa0936b86dcc2d2e91c kostenfrei http://www.sciencedirect.com/science/article/pii/S0022227520335835 kostenfrei https://doaj.org/toc/0022-2275 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2006 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 58 2017 7 1315-1324
allfields_unstemmed	10.1194/jlr.M073882 doi (DE-627)DOAJ055719996 (DE-599)DOAJbbaf1b6f3bb64fa0936b86dcc2d2e91c DE-627 ger DE-627 rakwb eng QD415-436 Nuntakorn Thongtang verfasserin aut Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL. lipoproteins/kinetics LDL subfractions statins dyslipidemia atherosclerosis mass spectrometry Biochemistry Margaret R. Diffenderfer verfasserin aut Esther M.M. Ooi verfasserin aut P. Hugh R. Barrett verfasserin aut Scott M. Turner verfasserin aut Ngoc-Anh Le verfasserin aut W. Virgil Brown verfasserin aut Ernst J. Schaefer verfasserin aut In Journal of Lipid Research Elsevier, 2021 58(2017), 7, Seite 1315-1324 (DE-627)26601593X (DE-600)1466675-3 15397262 nnns volume:58 year:2017 number:7 pages:1315-1324 https://doi.org/10.1194/jlr.M073882 kostenfrei https://doaj.org/article/bbaf1b6f3bb64fa0936b86dcc2d2e91c kostenfrei http://www.sciencedirect.com/science/article/pii/S0022227520335835 kostenfrei https://doaj.org/toc/0022-2275 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2006 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 58 2017 7 1315-1324
allfieldsGer	10.1194/jlr.M073882 doi (DE-627)DOAJ055719996 (DE-599)DOAJbbaf1b6f3bb64fa0936b86dcc2d2e91c DE-627 ger DE-627 rakwb eng QD415-436 Nuntakorn Thongtang verfasserin aut Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL. lipoproteins/kinetics LDL subfractions statins dyslipidemia atherosclerosis mass spectrometry Biochemistry Margaret R. Diffenderfer verfasserin aut Esther M.M. Ooi verfasserin aut P. Hugh R. Barrett verfasserin aut Scott M. Turner verfasserin aut Ngoc-Anh Le verfasserin aut W. Virgil Brown verfasserin aut Ernst J. Schaefer verfasserin aut In Journal of Lipid Research Elsevier, 2021 58(2017), 7, Seite 1315-1324 (DE-627)26601593X (DE-600)1466675-3 15397262 nnns volume:58 year:2017 number:7 pages:1315-1324 https://doi.org/10.1194/jlr.M073882 kostenfrei https://doaj.org/article/bbaf1b6f3bb64fa0936b86dcc2d2e91c kostenfrei http://www.sciencedirect.com/science/article/pii/S0022227520335835 kostenfrei https://doaj.org/toc/0022-2275 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2006 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 58 2017 7 1315-1324
allfieldsSound	10.1194/jlr.M073882 doi (DE-627)DOAJ055719996 (DE-599)DOAJbbaf1b6f3bb64fa0936b86dcc2d2e91c DE-627 ger DE-627 rakwb eng QD415-436 Nuntakorn Thongtang verfasserin aut Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL. lipoproteins/kinetics LDL subfractions statins dyslipidemia atherosclerosis mass spectrometry Biochemistry Margaret R. Diffenderfer verfasserin aut Esther M.M. Ooi verfasserin aut P. Hugh R. Barrett verfasserin aut Scott M. Turner verfasserin aut Ngoc-Anh Le verfasserin aut W. Virgil Brown verfasserin aut Ernst J. Schaefer verfasserin aut In Journal of Lipid Research Elsevier, 2021 58(2017), 7, Seite 1315-1324 (DE-627)26601593X (DE-600)1466675-3 15397262 nnns volume:58 year:2017 number:7 pages:1315-1324 https://doi.org/10.1194/jlr.M073882 kostenfrei https://doaj.org/article/bbaf1b6f3bb64fa0936b86dcc2d2e91c kostenfrei http://www.sciencedirect.com/science/article/pii/S0022227520335835 kostenfrei https://doaj.org/toc/0022-2275 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2006 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 58 2017 7 1315-1324
language	English
source	In Journal of Lipid Research 58(2017), 7, Seite 1315-1324 volume:58 year:2017 number:7 pages:1315-1324
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spellingShingle	Nuntakorn Thongtang misc QD415-436 misc lipoproteins/kinetics misc LDL subfractions misc statins misc dyslipidemia misc atherosclerosis misc mass spectrometry misc Biochemistry Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin
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topic	misc QD415-436 misc lipoproteins/kinetics misc LDL subfractions misc statins misc dyslipidemia misc atherosclerosis misc mass spectrometry misc Biochemistry
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title	Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin
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title_sort	metabolism and proteomics of large and small dense ldl in combined hyperlipidemia: effects of rosuvastatin
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title_auth	Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin
abstract	Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL.
abstractGer	Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL.
abstract_unstemmed	Small dense LDL (sdLDL) has been reported to be more atherogenic than large buoyant LDL (lbLDL). We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. Rosuvastatin enhances the catabolism of apoB-100 in both lbLDL and sdLDL.
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title_short	Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin
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We examined the metabolism and protein composition of sdLDL and lbLDL in six subjects with combined hyperlipidemia on placebo and rosuvastatin 40 mg/day. ApoB-100 kinetics in triglyceride-rich lipoproteins (TRLs), lbLDL (density [d] = 1.019–1.044 g/ml), and sdLDL (d = 1.044–1.063 g/ml) were determined in the fed state by using stable isotope tracers, mass spectrometry, and compartmental modeling. Compared with placebo, rosuvastatin decreased LDL cholesterol and apoB-100 levels in TRL, lbLDL, and sdLDL by significantly increasing the fractional catabolic rate of apoB-100 (TRL, +45%; lbLDL, +131%; and sdLDL, +97%), without a change in production. On placebo, 25% of TRL apoB-100 was catabolized directly, 37% was converted to lbLDL, and 38% went directly to sdLDL; rosuvastatin did not alter these distributions. During both phases, sdLDL apoB-100 was catabolized more slowly than lbLDL apoB-100 (P < 0.01). Proteomic analysis indicated that rosuvastatin decreased apoC-III and apoM content within the density range of lbLDL (P < 0.05). In our view, sdLDL is more atherogenic than lbLDL because of its longer plasma residence time, potentially resulting in more particle oxidation, modification, and reduction in size, with increased arterial wall uptake. 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Metabolism and proteomics of large and small dense LDL in combined hyperlipidemia: effects of rosuvastatin

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