Sduringthemetabolicstudy.Hyperlipidemicsubjectsoftenhave delayedLDLapoB-100catabolism(seesupplementalTable S3).Wehavedocumentedalsothatfeedingresultsinmore directTRLapoB-100catabolismandlessconversionofTRL apoB-100toLDLapoB-100,aswellasdelayedLDLapoB-100 catabolism,comparedwiththefastingstate(29).In spite of thedifferences,ourfindingsareconsistentwiththesepreviousstudiesandsupporttheconceptthatapoBinsdLDLs iscatabolizedmoreslowlythanapoBinlbLDLs. Our data indicate that approximately 80 of lbLDL apoB-100isderivedfromTRLapoB-100,withtheremainderMetabolism and proteomics of LDL subfractionsTABLE three. ApolipoproteincompositionoflbLDLandsdLDLduringplaceboandtreatmentwithrosuvastatin40mg/dayPlacebo(totalproteinspectralintensity,logbase2) Proteins lbLDL sdLDL PbRosuvastatin(totalproteinspectralintensity,logbase2) lbLDL sdLDL PbRosuvastatinvs.placebo,achange, (P) lbLDL sdLDLApoA-I ApoA-II ApoA-IV ApoC-I ApoC-II ApoC-III ApoC-IV ApoD ApoE ApoF ApoM19.9.9 19.0.five 0 9.1.six 22.0.1 23.4.3 ten.1.1 12.eight.two 23.5.1 11.7.8 18.five.22.8.5 19.3.7 14.7.7 19.eight.0 20.three.9 23.4.four 13.3.3 20.7.four 22.7.four 21.1.6 19.7.0.03 0.72 0.02 0.16 0.11 0.93 0.64 0.21 0.53 0.13 0.20.4.9 7.9.eight 0 7..9 20.2.eight 21.8.5 three.three.3 12.five.1 22.three.8 11.six.7 3.eight.22.9.5 19.2.three 14.1.5 19.8.6 20.four.4 23.five.two 13.four.four 20.5.4 22.5.four 20.9.two 18.8.0.09 0.08 0.02 0.07 0.78 0.02 0.07 0.19 0.92 0.12 0.two.6 (0.64) 58.1 (0.08) 0 two.1 (0.87) eight.two (0.11) 6.9 (0.04) 40.six (0.17) 1.three (0.07) 5.six (0.30) 0.six (0.79) 80.2 (0.02)0.eight (0.74) 0.two (0.88) three.1 (0.04) 0.7 (0.97) 1.3 (0.94) 0.four (0.92) 0.1 (0.95) 1.3 (0.46) 0.six (0.81) 0.7 (0.70) three.6 (0.43)Dataarepresentedasthetotalproteinspectralintensity,logbase2,oftheindividualproteins,ascalculatedbyAgilentSpectrumMill(Agilent Technologies),mean EM,n=5. a PercentchangerelativetoplacebowascalculatedonanindividualbasisandsummarizeddescriptivelybyLDLsubfraction.Significancefor comparisonofrosuvastatinphaseabsolutevalueswithplacebophaseabsolutevalueswasdeterminedbyusingapairedt-test. b SignificanceforcomparisonofsdLDLwithlbLDLwasdeterminedbyusingapairedt-test.getting produced straight. In addition they show that approximately 60 of sdLDL apoB-100 is derived from lbLDL apoB-100,withmostoftheremaindercomingdirectlyfrom TRLapoB-100.Theredoesappeartobeasmallpercentage ofsdLDLapoB-100derivedfromdirectliverproduction. Thesepercentagesarenotgreatlyalteredwithrosuvastatin therapyforeitherlbLDLapoB-100orsdLDLapoB-100.In thisstudy,wedidnotsubfractionatetheTRLfraction,and, consequently,wewereunabletoascertainwhichportionofthe TRLfractionmayhavebeentheprecursorof,orcontributed much more to, the sdLDL fraction, compared using the lbLDLfractionorhowrosuvastatinmayhavemodifiedthe delipidationcascademorespecifically.FGF-9 Protein custom synthesis Aguilar-Salinasetal.Hemoglobin subunit zeta/HBAZ Protein Storage & Stability (27) concluded that “a clear precursor-product relationship”wasobservedbetweentheVLDL,IDL,lightLDLand denseLDLfractions.PMID:34337881 Incontrast,Zhengetal.(28)discovered that 83 of sdLDL apoB-100 was derived straight from IDLs, with only eight getting derived from lbLDLs. Packard andcolleagues(302)didnotexaminethemetabolismof LDLsubfractionsdirectly;nevertheless,theydidproposethat, in subjects with moderate hypertriglyceridemia, there’s likelytobeincreasedconversionoflargeVLDLapoB-100 directlytosdLDL.Itshouldbenotedthattheseparationof LDL subfractions likely results inside the isolation of heterogeneous populations of particles that have unique metabolic and, hence, kinetic properties. Itwasimportanttoexaminedifferencesintheproteome oflbLDLsandsdLDLsonbothplaceboandrosuvastatin, whichpotentiallymightexplainthedifferenceinthec.