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Cited by 35Cholesterol and Lipid MetabolismLipoproteins and Cardiovascular HealthLipid metabolism and disorders

Plasma turnover of HDL apoC-I, apoC-III, and apoE in humans

Open access
Cohn, Jeffrey S., Batal, Rami, Tremblay, Michel, Jacques, Hélène, Veilleux, Lyne, Rodriguez, Claudia, Mamer, Orval, Davignon, Jean·2003·Journal of Lipid Research
DOI 10.1194/jlr.m300209-jlr200
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Abstract

Numerous factors are known to affect the plasma metabolism of HDL, including lipoprotein receptors, lipid transfer protein, lipolytic enzymes and HDL apolipoproteins. In order to better define the role of HDL apolipoproteins in determining plasma HDL concentrations, the aims of the present study were: a) to compare the in vivo rate of plasma turnover of HDL apolipoproteins [i.e., apolipoprotein A-I (apoA-I), apoC-I, apoC-III, and apoE], and b) to investigate to what extent these metabolic parameters are related to plasma HDL levels. We thus studied 16 individuals with HDL cholesterol levels ranging from 0.56-1.66 mmol/l and HDL apoA-I levels ranging from 89-149 mg/dl. Plasma kinetics of HDL apolipoproteins were investigated using a primed constant (12 h) infusion of deuterated leucine. Plasma HDL apolipoprotein levels were 41.8 +/- 1.5, 9.7 +/- 0.5, 4.9 +/- 0.5, and 0.7 +/- 0.1 micromol/l for apoA-I, apoC-I, apoC-III and apoE. Plasma transport rates (TRs) were 388.6 +/- 24.7, 131.5 +/- 12.5, 66.5 +/- 9.1, and 31.4 +/- 3.3 nmol.kg-1.day-1; and residence times (RTs) were 5.1 +/- 0.4, 3.7 +/- 0.3, 3.6 +/- 0.3, and 1.1 +/- 0.1 days, respectively. HDL cholesterol and apoA-I levels were significantly correlated with HDL apoA-I RT (r = 0.69 and r = 0.56), and were not significantly correlated with HDL apoA-I TR. In contrast, HDL apoC-I, apoC-III, and apoB levels were all positively related to their TRs and not their RTs. HDL apoC-III TR was positively correlated with levels of HDL apoC-III (r = 0.73, P < 0.01), and with those of HDL cholesterol and apoA-I (r = 0.54 and r = 0.53, P < 0.05, respectively). HDL apoC-III TR was in turn related to HDL apoA-I RT (r = 0.51, P < 0.05). Together, these results provide in vivo evidence for a link between the metabolism of HDL apoC-III and apoA-I, and suggest a role for apoC-III in the regulation of plasma HDL levels.

AI snapshot

Written from the paper’s full text.

TL;DR

In 16 humans, HDL apolipoprotein turnover differed markedly: apoA-I levels tracked with residence time, while apoC-I, apoC-III, and apoE levels tracked with transport rates. HDL apoC-III transport was linked to HDL cholesterol/apoA-I and apoA-I residence time, suggesting apoC-III may regulate plasma HDL levels.

Key findings

  • HDL apolipoprotein molar ratio was 1:7:14:60 (apoE/apoC-III/apoC-I/apoA-I); molar transport-rate ratio was 1:2:4:12. Residence times were 1.1 ± 0.1, 3.6 ± 0.3, 3.7 ± 0.3, and 5.1 ± 0.4 days for apoE, apoC-III, apoC-I, and apoA-I, respectively; fractional catabolic rates were 0.91, 0.28, 0.27, and 0.20 pools/day.
  • HDL apoA-I and HDL cholesterol levels correlated with HDL apoA-I residence time (r = 0.56 and r = 0.69) and not with apoA-I transport rate. In contrast, HDL apoC-I, apoC-III, and apoE levels were positively related to their transport rates (r = 0.62, r = 0.73, r = 0.66, respectively) and not their residence times.
  • HDL apoC-III transport rate correlated with HDL apoC-III (r = 0.73, P < 0.01), HDL cholesterol (r = 0.54, P < 0.05), HDL apoA-I (r = 0.53, P < 0.05), and HDL apoA-I residence time (r = 0.51, P < 0.05). Similar relationships were not observed for HDL apoC-I or HDL apoE.

Methods

  • Retrospective analysis of stored plasma from 16 subjects (15 males, 1 female; aged 25–67 years; BMI 23.5–30.2 kg/m²; HDL cholesterol 0.56–1.66 mmol/l; apoA-I 89–149 mg/dl) who had participated in prior stable-isotope kinetic studies.
  • Subjects received a primed constant 12 h intravenous infusion of deuterated leucine; blood samples were collected over 12 h. Lipoproteins were isolated by sequential ultracentrifugation, and apoA-I, apoC-I, apoC-III, and apoE were separated by preparative electrophoresis or isoelectric focusing; concentrations were measured by nephelometry or ELISA, and isotopic enrichment by GC-MS.
  • Kinetic data were fitted to a three-compartment model using SAAM II to derive fractional transport rates, residence time (1/FTR), and transport rate. Pearson correlations and paired Student’s t-tests with Bonferroni correction were used.

Limitations

  • Stated: plasma leucine was used as the precursor pool rather than VLDL apoB-100 plateau; because plasma leucine plateau is usually 10–15% higher than VLDL apoB-100, this may have caused a 10–15% underestimation of fractional catabolic rates for all apolipoproteins.
  • Stated/assumption: apoC-I, apoC-III, and apoE recovered in the d > 1.21 g/ml fraction were included as HDL apolipoproteins; for apoE this represented 14.6 ± 0.9% of total apoE, and the authors argue it reflects apoE stripped from HDL during ultracentrifugation.
  • Evident: small sample (n = 16; 15 male/1 female), retrospective design, and correlational analysis cannot establish causality; possible ultracentrifugation artifacts and HDL particle heterogeneity may affect interpretation.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1194/jlr.m300209-jlr200

Cites

51 of 51 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

4 of 18 cited sources checked · 1 supported · 0 flagged · accuracy not yet measured

  • Interpretationown data

    Catabolism rather than production is the major determinant of HDL apoA-I levels.

    “These data suggest that catabolism rather than production is the major determinant of HDL apoA-I levels, as suggested by previous studies (43)(44)(45).”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [43] Schaefer, 1982, Human apolipoprotein A-I and A-II metabolism, J. Lipid Res. source
    • cites [44] Horowitz, 1993, Increased plasma and renal clearance of an exchangeable pool of apolipoprotein A-I in subjects with low levels of high density lipoprotein cholesterol, J. Clin. Invest. source
    • cites [45] Brinton, 1994, Human HDL cholesterol levels are determined by apoA-I fractional catabolic rate, which correlates inversely with estimates of HDL particle size. Effects of gender, hepatic and lipoprotein lipases, triglyceride and insulin levels, and body fat distribution, Arterioscler. Thromb. source

      The Discussion (page not available in our copy) says apoA-I fractional catabolic rate predicts variation in HDL cholesterol better than apoA-I production or transport rate. The claim instead concerns apoA-I levels; the same section notes a study suggesting that production rate may predict those levels better than catabolic rate. This paper therefore supports the comparison for HDL cholesterol, but not for the stated outcome. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Findingown data

    Plasma transport rates of HDL apolipoproteins were 388.6 ±24.7, 131.5 ±12.5, 66.5 ±9.1, and 31.4 ±3.3 nmol/kg/day for apoA-I, apoC-I, apoC-III, and apoE, respectively.

    “Plasma transport rates (TRs) were 388.6 ؎ 24.7, 131.5 ؎ 12.5, 66.5 ؎ 9.1, and 31.4 ؎ 3.3 nmol•kg ؊ 1 •day ؊ 1 ; and residence times (RTs) were 5.1 ؎ 0.4, 3.7 ؎ 0.3, 3.6 ؎ 0.3, and 1.1 ؎ 0.1 days, respectively.”
    Quote in the paperSubstantial claim
  • Findingown data

    HDL apoC-III TR was related to HDL apoA-I RT (r=0.51, P<0.05).

    “HDL apoC-III TR was in turn related to HDL apoA-I RT ( r ‫؍‬ 0.51, P Ͻ 0.05).”
    • Also stated in: § Relationship between HDL apolipoprotein levels and kinetic parameters · plain
      “Importantly, HDL apoC-III TRs were postively correlated with both HDL cholesterol and apoA-I levels (r ϭ 0.54 and r ϭ 0.53, P Ͻ 0.05, respectively), and HDL apoC-III TRs were in turn related to HDL apoA-I RTs (r ϭ 0.51, P Ͻ 0.05).”
    Quote in the paperSubstantial claim
  • Findingown data

    HDL apoC-III TR was positively correlated with HDL apoA-I levels (r=0.53, P<0.05).

    “Importantly, HDL apoC-III TRs were postively correlated with both HDL cholesterol and apoA-I levels (r ϭ 0.54 and r ϭ 0.53, P Ͻ 0.05, respectively), and HDL apoC-III TRs were in turn related to HDL apoA-I RTs (r ϭ 0.51, P Ͻ 0.05).”
    • Also stated in: § Abstract · plain
      “HDL apoC-III TR was postively correlated with levels of HDL apoC-III ( r ‫؍‬ 0.73, P Ͻ 0.01), and with those of HDL cholesterol and apoA-I ( r ‫؍‬ 0.54 and r ‫؍‬ 0.53, P Ͻ 0.05, respectively).”
    Quote in the paperSubstantial claim
  • Findingown data

    HDL apoC-III TR was positively correlated with HDL cholesterol levels (r=0.54, P<0.05).

    “Importantly, HDL apoC-III TRs were postively correlated with both HDL cholesterol and apoA-I levels (r ϭ 0.54 and r ϭ 0.53, P Ͻ 0.05, respectively), and HDL apoC-III TRs were in turn related to HDL apoA-I RTs (r ϭ 0.51, P Ͻ 0.05).”
    • Also stated in: § Abstract · plain
      “HDL apoC-III TR was postively correlated with levels of HDL apoC-III ( r ‫؍‬ 0.73, P Ͻ 0.01), and with those of HDL cholesterol and apoA-I ( r ‫؍‬ 0.54 and r ‫؍‬ 0.53, P Ͻ 0.05, respectively).”
    Quote in the paperSubstantial claim
  • Classified as probably not a substantial claim. 5
  • May combine two claims. 21
  • The quote only partly states this claim. 1

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductcitation

    ApoC-I, apoC-III, and apoE recovered in the d>1.21 g/ml fraction were included in HDL fractions, which were corrected so that total apolipoprotein recovery after ultracentrifugation was 100%.

    “As explained before (24-26), apoC-I, apoC-III, and apoE recovered in the d Ͼ 1.21 g/ml fraction (1.9 Ϯ 0.4%, 0.5 Ϯ 0.1%, and 14.6 Ϯ 0.9% of total, respectively) were included in HDL fractions, which were in turn corrected so that total apolipoprotein recovery after ultracentrifugation was 100%.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [24] Batal, 2000, Plasma kinetics of apoC-III and apoE in normolipidemic and hypertriglyceridemic subjects, J. Lipid Res. source
    • cites [25] Cohn, 2002, Effect of atorvastatin on plasma apoE metabolism in patients with combined hyperlipidemia, J. Lipid Res. source

      The plasma lipids and apolipoproteins passage (indexed as Abstract; page unavailable) includes apoE from the d > 1.21 g/ml fraction in the recovery calculation and says final lipoprotein apoE concentrations were corrected to 100% recovery. It does not say that this fraction was included in HDL, or document the same procedure for apoC-I and apoC-III. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites [26] Cohn, 2002, Plasma kinetics of VLDL and HDL apoC-I in normolipidemic and hypertriglyceridemic subjects, J. Lipid Res. source

      The Methods section says apoC-I in the bottom fractions was counted in the HDL apoC-I pool and that lipoprotein apoC-I levels were corrected to 100% recovery. The Results section places less than 3% of apoC-I in the d > 1.21 g/ml fraction. This paper does not establish the corresponding treatment or quoted percentages for apoC-III and apoE, nor the exact 1.9 ± 0.4% figure for apoC-I. (LLM, conf=0.87)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Findingown data

    HDL cholesterol and apoA-I levels were significantly correlated with HDL apoA-I RT (r=0.69 and r=0.56), and were not significantly correlated with HDL apoA-I TR.

    “HDL cholesterol and apoA-I levels were significantly correlated with HDL apoA-I RT ( r ‫؍‬ 0.69 and r ‫؍‬ 0.56), and were not significantly correlated with HDL apoA-I TR.”
    • Also stated in: § Relationship between HDL apolipoprotein levels and kinetic parameters · plain
      “As expected from previous studies, HDL apoA-I and HDL cholesterol levels were significantly correlated with HDL apoA-I RTs (r ϭ 0.56 and r ϭ 0.69), and were not significantly correlated with HDL apoA-I TRs.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    HDL apoE levels were positively correlated with HDL apoE TR (r=0.66, P<0.01) and not with HDL apoE RT.

    “Positive relationships between TRs and HDL apoE, apoC-III, and apoC-I levels (r ϭ 0.66, P Ͻ 0.01; r ϭ 0.73, P Ͻ 0.01; and r ϭ 0.62, P Ͻ 0.05, respectively), are shown in Fig. 2, contrasting to data for apoA-I.”
    • Also stated in: § Relationship between HDL apolipoprotein levels and kinetic parameters · plain
      “In contrast, HDL apoE, apoC-III, and apoC-I levels were all positively related to their TRs and not their RTs.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Plasma HDL apolipoprotein levels were 41.8 ±1.5, 9.7 ±0.5, 4.9 ±0.5, and 0.7 ±0.1 mol/l for apoA-I, apoC-I, apoC-III, and apoE, respectively.

    “Plasma HDL apolipoprotein levels were 41.8 ؎ 1.5, 9.7 ؎ 0.5, 4.9 ؎ 0.5, and 0.7 ؎ 0.1 mol/l for apoA-I, apoC-I, apoC-III and apoE.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    HDL apoC-III levels were positively correlated with HDL apoC-III TR (r=0.73, P<0.01) and not with HDL apoC-III RT.

    “HDL apoC-III TR was postively correlated with levels of HDL apoC-III ( r ‫؍‬ 0.73, P Ͻ 0.01), and with those of HDL cholesterol and apoA-I ( r ‫؍‬ 0.54 and r ‫؍‬ 0.53, P Ͻ 0.05, respectively).”
    • Also stated in: § Relationship between HDL apolipoprotein levels and kinetic parameters · plain
      “Positive relationships between TRs and HDL apoE, apoC-III, and apoC-I levels (r ϭ 0.66, P Ͻ 0.01; r ϭ 0.73, P Ͻ 0.01; and r ϭ 0.62, P Ͻ 0.05, respectively), are shown in Fig. 2, contrasting to data for apoA-I.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    HDL apoC-I levels were positively correlated with HDL apoC-I TR (r=0.62, P<0.05) and not with HDL apoC-I RT.

    “Positive relationships between TRs and HDL apoE, apoC-III, and apoC-I levels (r ϭ 0.66, P Ͻ 0.01; r ϭ 0.73, P Ͻ 0.01; and r ϭ 0.62, P Ͻ 0.05, respectively), are shown in Fig. 2, contrasting to data for apoA-I.”
    • Also stated in: § Relationship between HDL apolipoprotein levels and kinetic parameters · plain
      “In contrast, HDL apoE, apoC-III, and apoC-I levels were all positively related to their TRs and not their RTs.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Residence times of HDL apolipoproteins were 5.1 ±0.4, 3.7 ±0.3, 3.6 ±0.3, and 1.1 ±0.1 days for apoA-I, apoC-I, apoC-III, and apoE, respectively.

    “Plasma transport rates (TRs) were 388.6 ؎ 24.7, 131.5 ؎ 12.5, 66.5 ؎ 9.1, and 31.4 ؎ 3.3 nmol•kg ؊ 1 •day ؊ 1 ; and residence times (RTs) were 5.1 ؎ 0.4, 3.7 ؎ 0.3, 3.6 ؎ 0.3, and 1.1 ؎ 0.1 days, respectively.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingreasoning

    HDL apolipoproteins have significantly different rates of transport and significantly different RTs.

    “In view of this particle heterogeneity, it is not surprising that HDL apolipoproteins have significantly different rates of transport and significantly different RTs (Table 2).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In molar terms, apoE had the lowest and apoA-I had the highest TR, and the ratio between TRs was 1:2:4:12 (apoE/apoC-III/apoC-I/apoA-I).

    “In molar terms, apoE had the lowest and apoA-I had the highest TR, and the ratio between TRs was 1:2:4:12 (apoE/apoC-III/apoC-I/ apoA-I).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    HDL apoE %ttr increased most rapidly, apoA-I %ttr increased least rapidly, and apoC-III and apoC-I were intermediate and virtually indistinguishable.

    “HDL apoE %ttr increased the most rapidly, apoA-I %ttr increased the least rapidly, and apoC-III and apoC-I were intermediate, and were virtually indistinguishable.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    HDL cholesterol and HDL apoA-I concentrations were significantly correlated (r=0.52, P<0.05).

    “HDL cholesterol and HDL apoA-I concentrations were significantly correlated (r ϭ 0.52, P Ͻ 0.05).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Plasma HDL apoE concentration was significantly lower than HDL apoC-III, which was lower than HDL apoC-I, which was lower than HDL apoA-I (P<0.01).

    “Plasma HDL apoE concentration (in mg/dl) was significantly lower than that of HDL apoC-III, which was in turn significantly lower than that of HDL apoC-I, which was in turn significantly lower than that of HDL apoA-I (P Ͻ 0.01).”
    Quote in the paperNot a substantial claim
    • The authors state this as an assumption: Any apoC-I, apoC-III, or apoE in the d>1.21 g/ml fraction was HDL apolipoprotein.

  • May combine two claims.

    Findingown data

    Each molecule of apoE remained in the HDL fraction for an average of one day, while each molecule of apoA-I remained in HDL for an average of 5 days.

    “Each molecule of apoE remained in the HDL fraction for an average of one day, while each molecule of apoA-I remained in HDL for an average of 5 days.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    HDL apoC-I, apoC-III, and apoE levels were significantly correlated with their transport rates (TRs) and not with their residence times (RTs).

    “while levels of HDL apoC-I, apoC-III, and apoE were significantly correlated with their TRs and not their RTs (Fig. 2).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    HDL apoA-I concentration was significantly correlated with its residence time (RT) and not with its transport rate (TR).

    “An interesting feature of the present data is that HDL apoA-I concentration was significantly correlated with RT and not with TR”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In terms of mg/kg/day, apoA-I had the highest rate of transport and HDL apoC-III had the lowest rate of transport, with HDL apoE and apoC-I being intermediate.

    “In terms of mg•kg Ϫ1 •day Ϫ1 , apoA-I had the highest rate of transport and HDL apoC-III had the lowest rate of transport, with HDL apoE and apoC-I being intermediate.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    ApoC-III is found in smaller (5-12 nm) α-migrating HDL.

    “ApoC-III on the other hand, like apoA-II, is found in smaller (5-12 nm) ␣-migrating HDL (36).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [36] Krimbou, 1997, Characterization of human plasma apolipoprotein E-containing lipoproteins in the high density lipoprotein size range: focus on pre-beta1-LpE, pre-beta2-LpE, and alpha-LpE, J. Lipid Res. source

  • May combine two claims.

    Interpretationcitation

    The present study's HDL apoA-I TR (11.0 ±0.7 mg/kg/day) and HDL apoA-I RT (5.1 ±0.4 days) compare very well with previous stable-isotope data.

    “These data compare very well with those obtained for apoA-I in the present study (i.e., HDL apoA-I TR: 11.0 Ϯ 0.7 mg•kg Ϫ1 •day Ϫ1 and HDL apoA-I RT: 5.1 Ϯ 0.4 days).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [37] Marsh, 2000, Stable isotope turnover of apolipoproteins of high-density lipoproteins in humans, Curr. Opin. Lipidol. source

  • May combine two claims.

    Premisecitation

    In the previous apoC-I kinetic study by Malmendier et al., for four NL subjects, apoC-I TR was 1.8 mg/kg/day and RT was 3.2 days.

    “More than 80% of injected 125 I-BH-apoC-I was found associated in plasma with HDL (38), and for four NL subjects, apoC-I TR was determined to be 1.8 mg•kg Ϫ1 •day Ϫ1 and RT was 3.2 days, which compares to 0.9 Ϯ 0.1 mg•kg Ϫ1 •day Ϫ1 and 3.7 Ϯ 0.3 days, respectively, in the present study.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [38] Malmendier, 1986, Metabolism of apolipoprotein C–I in normolipoproteinemic human subjects, Atherosclerosis. source

  • May combine two claims.

    Interpretationreasoning

    Some HDL particles evidently contain more than one exchangeable apolipoprotein, or alternatively more than one copy of apoC-I, apoC-III, and/or apoE.

    “Some HDL particles evidently contain more than one exchangeable apolipoprotein, or alternatively more than one copy of apoC-I, apoC-III, and/or apoE.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    Assuming two to four molecules of apoA-I in each HDL particle, the data suggest that less than 10% of all HDL particles in the circulation contain apoE, less than half contain apoC-I, and about two-thirds contain apoC-III.

    “Assuming that there are two to four molecules of apoA-I in each HDL particle, the aforementioned data suggest that less than 10% of all HDL particles in the circulation contain apoE, less than half contain apoC-I, and about two-thirds contain apoC-III.”
    Quote in the paperSubstantial claim
    • The authors state this as an assumption: There are two to four molecules of apoA-I in each HDL particle.

  • May combine two claims.

    Study design and conductown data

    Plasma apoA-I concentrations were taken to represent HDL apoA-I levels because >90% of plasma apoA-I was consistently found in the HDL fraction after ultracentrifugation.

    “Because Ͼ 90% of plasma apoA-I was consistently found in the HDL fraction after ultracentrifugation (1.063 Ͻ d Ͻ 1.21 g/ml), plasma apoA-I concentrations were taken to represent HDL apoA-I levels.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    HDL apolipoproteins are kinetically as well as dynamically different.

    “and that HDL apolipoproteins are kinetically as well as dynamically different.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). The quote only partly states this claim.

    Study design and conductown data

    Intraassay and interassay coefficients of variation for apoC-I, apoC-III, and apoE ELISAs were between 2% and 10%.

    “Intraassay and interassay coefficients of variation were between 2% and 10%.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    The difference may reflect that 125I-labeled apoE can exchange or transfer more readily from HDL to VLDL than endogenously labeled apoE.

    “which may reflect the fact that 125 I-labeled apoE can exchange or transfer more readily from HDL to VLDL than endogenously labeled apoE.”
    Quote in the paperNot a substantial claim
25 of 25

  • The authors state this as an assumption.

    Any apoC-I, apoC-III, or apoE in the d>1.21 g/ml fraction was HDL apolipoprotein.

    “In obtaining these ratios, it is important to note that we have assumed that any apoC-I, apoC-III, or apoE in the d Ͼ 1.21 g/ml fraction was HDL apolipoprotein.”

  • The authors state this as an assumption.

    There are two to four molecules of apoA-I in each HDL particle.

    “Assuming that there are two to four molecules of apoA-I in each HDL particle, the aforementioned data suggest that less than 10% of all HDL particles in the circulation contain apoE, less than half contain apoC-I, and about two-thirds contain apoC-III.”
2 of 2

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Abstract names apoB where the results name apoE

    Minor

    The abstract says HDL apoB levels were related to their transport rates, but the corresponding results identify apoE, not apoB, alongside apoC-I and apoC-III.

1 of 1

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Related

Authors
Cohn, J. S., Batal, R., Tremblay, M., Jacques, H., Veilleux, L., Rodriguez, C., Mamer, O., & Davignon, J.
Affiliations
  • Montreal Clinical Research Institute (CA)
  • McGill University (CA)
Corresponding author
Cohn, Jeffrey S.
ORCID
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2003-10
Volume
44
Issue
10
Pages
1976-1983
ISSN
0022-2275 (ISSN-L)
DOI
10.1194/jlr.m300209-jlr200
OpenAlex
W2103369120
Cited by
35
References
51
Citations by year
2024: 1 · 2023: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 1 · 2015: 2 · 2014: 1 · 2012: 3
FWCI
3.38
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Lipid Research (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Pfizer
  • Heart and Stroke Foundation of Canada
  • Pfizer Canada
Topics
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Keywords
HDL apolipoproteins, apolipoprotein A-I, apolipoprotein C-I, apolipoprotein C-III, apolipoprotein E, HDL cholesterol, transport rate, residence time
MeSH terms
Adult, Aged, Apolipoproteins C, Apolipoproteins E, Cholesterol, Female, Humans, Isotope Labeling, Kinetics, Lipoproteins, Lipoproteins, HDL, Male, Middle Aged, Time Factors, Triglycerides, Apolipoprotein C-I, Apolipoprotein C-III

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Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-31.

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Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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