![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Department of Molecular and Nuclear Medicine, Life Sciences Division, Ernest Orlando Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
24% fat has been found
to represent a reduction in numbers of circulating mid-sized and small
LDL particles, and hence an expected lowering of cardiovascular disease
risk. In contrast, in the majority of healthy individuals with larger
LDL (pattern A, found in 
70% of men and a larger percentage of
women), a significant proportion of the low fat diet–induced reduction
in plasma LDL cholesterol is made by depletion of the cholesterol
content of LDL particles. This change in LDL composition is accompanied
by a shift from larger to smaller LDL particle diameters. Moreover,
with progressive reduction of dietary fat and isocaloric substitution
of carbohydrate, an increasing number of subjects with pattern A
convert to the pattern B phenotype. Studies in families have indicated
that susceptibility to induction of pattern B by low fat diets is under
genetic influence. Thus, diet-gene interactions affecting LDL
subclass patterns may contribute to substantial interindividual
variability in the effects of low fat diets on coronary heart disease
risk.
KEY WORDS: • cholesterol • LDL • diet • fat • carbohydrate • lipoprotein subclasses
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
, Schaefer et al. 1997
), with many showing either little change or even increases
in these parameters. Moreover, low fat, high carbohydrate diets can
also result in reduced plasma HDL cholesterol and/or increased
triglyceride, raising the possibility that these changes may offset to
varying degrees the expected benefit of LDL cholesterol lowering. The
wide interindividual variations in lipoprotein response to altered
dietary composition have been attributed at least in part to genetic
differences among individuals (Dreon and Krauss 1997
,
Ordovas 1999
, Schaefer et al., 1997
).
Although a number of studies have demonstrated associations of these
variations with polymorphisms in candidate genes (Dreon and Krauss 1997
, Ordovas 1999
), the magnitude of
these effects has generally been small, and it is likely that multiple
factors, many as yet unrecognized, are involved. |
Atherogenic lipoprotein phenotype |
|---|
|
TOPABSTRACTINTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
).
Moreover, there is variation in the distribution of these subclasses
among individuals. In the majority of healthy subjects, the major forms
of LDL are large and buoyant, but in a substantial subset of the
population, there is a predominance of small, dense LDL particles
(Austin et al. 1990
). The small, dense LDL profile,
designated LDL subclass pattern B, is associated with relative
increases in plasma triglyceride and other proatherogenic metabolic
changes, including increased intermediate density lipoproteins, reduced
HDL cholesterol (Austin et al. 1990
) and reduced insulin
sensitivity (Reaven et al. 1993
). Moreover, small LDL
particles appear to have greater atherogenic potential than large LDL
by virtue of reduced receptor-mediated clearance (Campos et al. 1996
) and higher endothelial transport (Nielsen 1996
), proteoglycan binding (Anber et al. 1997
)
and oxidative susceptibility (Tribble et al. 1992
).
Overall, this profile can result in approximately a threefold increase
in risk for coronary artery disease (Austin et al. 1988
,
Gardner et al. 1996
, Lamarche et al. 1997
, Stampfer et al. 1996
), an observation that
supports its designation as an atherogenic lipoprotein phenotype. The
magnitude of the risk, however, is strongly dependent on overall plasma
concentrations of apolipoprotein (apo)B-containing lipoproteins,
suggesting that the quantity as well as the quality of LDL subfractions
should be considered in assessing atherosclerosis risk. |
Genetic influences on LDL subclasses |
|---|
|
TOPABSTRACTINTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
,
Austin 1994
); linkages of LDL particle size phenotypes
to several candidate gene loci have been reported (Allayee et al. 2000
, Austin et al. 1998
, Nishina et al. 1992
, Rotter et al. 1996
, Talmud et al. 2000
). To date, the most consistent evidence for linkage
has been found for a locus in the vicinity of the LDL receptor gene on
chromosome 19p (Nishina et al. 1992
, Rotter et al. 1996
), the apoCIII gene locus on chromosome 11
(Allayee et al. 1998
, Rotter et al. 1996
)
and the cholesteryl ester transfer protein gene on chromosome 16
(Rotter et al. 1996
, Talmud et al. 2000
).
Thus, major genes may act singly or in combination to influence LDL
particle size. Although a number of the linked genes have a plausible
basis for contributing to variation in LDL subclass profiles, in the
case of the LDL receptor gene, analyses of DNA sequences in the coding
region (Naggert et al. 1997
) as well as immediately
upstream (Naggert, J.K., Nishina, P.M., Krauss, R.M., personal
communication) showed no significant differences in pattern B vs.
pattern A subjects from informative families. Coupled with the
observation of normal LDL receptor function in fibroblasts of pattern B
subjects (Campos et al. 1996
), these findings rule out
an LDL receptor structural variant in the etiology of pattern B, but do
not rule out an abnormality related to regulation of this gene. |
Gene-diet interactions involving small dense LDL |
|---|
|
TOPABSTRACTINTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
, Lamon-Fava et al. 1991
). This is
consistent with the strong influence of modifying factors on the
expression of LDL subclass pattern B. Age and gender are major
determinants, with a prevalence of 30% in men, 15–20% in
postmenopausal women and 5–10% in younger individuals (Austin et al. 1990
and 1993
, Campos et al. 1992
). In
addition, LDL size is influenced by metabolic factors affecting plasma
triglyceride (Krauss et al. 1988
, McNamara et al. 1987
), including abdominal adiposity (Terry et al. 1989
) and insulin resistance (Reaven et al. 1993
). Given the evidence for differences in the metabolic and pathologic behavior among LDL subclasses and for both genetic and environmental influences on LDL particle profiles, we have sought to determine whether diets designed to lower LDL cholesterol have different effects on LDL subclasses and whether genetic factors underlying susceptibility to the atherogenic lipoprotein phenotype contribute to interindividual variability in lipoprotein response to such diets.
Initial observations were made in a cohort of 105 healthy nonobese
normolipidemic men who consumed high (46% of energy) and low fat (24%
of energy) diets for 6 wk each in a randomized, crossover design
(Dreon et al. 1994
, Krauss and Dreon 1995
). Differences in composition of the diets involved
proportional changes in both saturated and polyunsaturated fat with
reciprocal changes in carbohydrate (equally distributed between sugar
and starch); no change in content of monounsaturated fat, protein,
cholesterol or fiber; and adjustment of energy to maintain constant
body weight. Compared with the high fat diet, the low fat diet resulted
in a significant mean reduction in LDL cholesterol of 11%, consistent
with the difference predicted from equations described previously
(Hegsted et al. 1993
, Keys 1957
).
However, the distribution of values was broad (Fig. 1
), with a range from -49 to +51%.
|
,
Krauss and Dreon 1995
). This was associated with
significantly greater reductions in mass of mid-sized (LDL 2) and
small (LDL 3) LDL subfractions measured by analytic ultracentrifugation
(Krauss and Dreon 1995
). Furthermore, only pattern B
subjects showed significant reductions in plasma apoB, and in LDL
relative to HDL cholesterol levels (Dreon et al. 1994
).
Of the 87 men with pattern A consuming the high fat diet, 36 converted
to pattern B when consuming the low fat diet (Dreon et al. 1994
). In these men, there was a shift in LDL particle mass
from larger, lipid-enriched (LDL1 and 2) to smaller,
lipid-depleted (LDL 3 and 4) subfractions (Krauss and Dreon 1995
), suggestive of change in LDL composition with minimal
change in particle number, and consistent with the observation of
reduced plasma LDL cholesterol without reduced plasma apoB. The group
differences in LDL and apoB response could not be attributed to
differences in plasma lipid levels or body mass indices or to apoE
phenotypes. Increases in plasma triglyceride and reductions in HDL
cholesterol with the low fat, high carbohydrate diet were comparable in
pattern A and B subjects (Dreon et al. 1994
). Taken
together, these results indicate that in the majority of men, the
reduction in LDL cholesterol seen during consumption of a low fat, high
carbohydrate diet is due in large measure to a shift from larger, more
cholesterol-enriched LDL to smaller, cholesterol-depleted LDL,
whereas much greater reductions in LDL cholesterol and a reduction in
the number of smaller LDL particles are achieved in individuals with a
predominance of small, dense LDL consuming a high fat diet.
These results, which have been confirmed in a second study in 133 men
(Dreon and Krauss 1995
), indicate that reduction in
dietary fat and increase in carbohydrate can elicit the expression of
LDL subclass pattern B in a subset of healthy men. Moreover, a
short-term (10 d) dietary challenge of a 10% fat diet in 38
healthy men with pattern A consuming diets containing 20–24% fat
resulted in a conversion to pattern B in 12 men (32%) (Dreon et al. 1999
). There were no significant reductions in LDL
cholesterol levels in the group as a whole, but those who converted to
pattern B had significantly greater increases in levels of triglyceride
and apoB and reductions in HDL cholesterol than those who remained
pattern A (Dreon et al. 1999
).
Overall, in a series of such studies employing diets with varying fat
content and reciprocal variation in carbohydrate content, there is a
strong linear relationship of decreased fat/increased carbohydrate
intake with prevalence of LDL subclass pattern B in healthy men
(Fig. 2
). These results indicate that the prevalence of pattern B in men
consuming 30% fat is 30–35%, a figure that is consistent with the
prevalence of pattern B in men in the general population (Austin et al. 1990
, Campos et al. 1992
). Hence, the
results suggest that the short-term effects of variation in diet
composition on LDL subclass phenotypes are indicative of the effects of
long-term diet consumption.
|
|
Genetic influences on response of LDL subclass patterns to low fat diet |
|---|
|
TOPABSTRACTINTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
indicate that dietary fat and/or
carbohydrate intake are strong determinants of subclass pattern B, and
may act to induce expression of this trait in susceptible individuals.
Moreover, given the evidence for genetic effects on LDL subclass
patterns, the results raise the possibility that induction of pattern B
by a low fat, high carbohydrate diet is also under genetic influence.
Heritability of this diet response has been demonstrated in two family
studies involving premenopausal women (Dreon et al. 1997
) and children (Dreon et al. 2000
), groups
with low expression of pattern B in whom genetic susceptibility to this
trait was inferred by its presence in one or both parents. In both
studies, prevalence of pattern B after consumption of a low fat diet
was greatest in offspring of two pattern B parents.
On the basis of the evidence for heritability of induction of pattern B
by a low fat diet, we hypothesized that one or more of the genes linked
to variation in LDL particle size may be responsible for this diet
effect. To test this hypothesis, we recently studied the effects of
reduction in dietary fat from 40 to 20% of energy in a cohort of 298
brothers from 135 families in whom linkage to a polymorphism in the LDL
receptor was tested by nonparametric sibpair linkage analysis
(Krauss et al. 1999
). Significant linkage was observed
during consumption of both high and low fat diets, confirming earlier
results in families in whom diet was not controlled. No genetic linkage
was found for other lipid or lipoprotein variables, except for HDL
cholesterol, which showed weak linkage to the LDL receptor gene
(P < 0.05) for both diets. Interestingly, linkage of
LDL subclass pattern (qualitative phenotype) was stronger with
consumption of the high fat diet, whereas linkages of quantitative
measures (LDL density and size) were stronger with consumption of the
low fat diet. Most notably, the tendency for a low fat diet to induce
expression of LDL subclass pattern B was also linked to the LDL
receptor gene. It therefore appears that the genetic locus on
chromosome 19p that influences LDL subclass pattern with consumption of
a high fat diet also contributes to susceptibility for reduced size and
increased density of LDL particles, and induction of the pattern B
phenotype during consumption of a low fat diet. Thus, it is likely that
one or more genes at this locus underlie diet-gene interactions
affecting LDL subclass phenotypes.
|
SUMMARY |
|---|
|
TOPABSTRACTINTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
). In the case of genes influencing LDL subclass patterns,
gene-diet interactions contribute to wide interindividual
differences in the effects of low fat, high carbohydrate diets on risk
for coronary heart disease. The recognition of such differences in
metabolic response is prompting greater attention to the potential for
individualization of nutritional approaches for prevention of heart
disease (Krauss et al. 1996). Once specific genes
responsible for these effects are identified, it will be possible to
use this information to target low fat dietary interventions more
effectively to those individuals most likely to achieve a benefit for
cardiovascular disease risk (Krauss 2000
).
|
FOOTNOTES |
|---|
2 Supported by the National Institutes of Health Program Project Grant HL 18574 from the National Heart, Lung, and Blood Institute, a grant from the National Dairy Promotion and Research Board; the study was administered in cooperation with the National Dairy Council and was conducted at the Ernest Orlando Lawrence Berkeley National Laboratory through the U.S. Department of Energy under Contract No. DE-AC03–76SF00098.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONAtherogenic lipoprotein...Genetic influences on LDL...Gene-diet interactions involving...Genetic influences on response...SUMMARYREFERENCES |
|---|
1. Allayee H., Aouizerat B. E., Cantor R. M., Dallinga-Thie G. M., Krauss R. M., Lanning C. D., Rotter J. I., Lusis A. J., de Bruin T. W. Families with familial combined hyperlipidemia and families enriched for coronary artery disease share genetic determinants for the atherogenic lipoprotein phenotype. Am. J. Hum. Genet. 1998;63:577-585[Medline]
2.
Allayee H., Dominguez K. M., Aouizerat B. E., Krauss R. M., Rotter J. I., Lu J., Cantor R. M., de Bruin T. W., Lusis A. J. Contribution of the hepatic lipase gene to the atherogenic lipoprotein phenotype in familial combined hyperlipidemia. J. Lipid Res. 2000;41:245-252
3.
Anber V., Millar J. S., McConnell M., Shepherd J., Packard C. J. Interaction of very-low-density, intermediate-density, and low-density lipoproteins with human arterial wall proteoglycans. Arterioscler. Thromb. Vasc. Biol. 1997;17:2507-2514
4. Austin M. A. Genetic and environmental influences on LDL subclass phenotypes. Clin. Genet. 1994;46:64-70[Medline]
5. Austin M. A., Breslow J. L., Hennekens C. H., Buring J. E., Willett W. C., Krauss R. M. Low-density lipoprotein subclass patterns and risk of myocardial infarction. J. Am. Med. Assoc. 1988;260:1917-1921[Abstract]
6.
Austin M. A., King M. C., Vranizan K. M., Krauss R. M. Atherogenic lipoprotein phenotype. A proposed genetic marker for coronary heart disease risk [see comments]. Circulation 1990;82:495-506
7. Austin M. A., King M. C., Vranizan K. M., Newman B., Krauss R. M. Inheritance of low-density lipoprotein subclass patterns: results of complex segregation analysis. Am. J. Hum. Genet. 1988;43:838-846[Medline]
8.
Austin M. A., Newman B., Selby J. V., Edwards K., Mayer E. J., Krauss R. M. Genetics of LDL subclass phenotypes in women twins. Concordance, heritability, and commingling analysis. Arterioscler. Thromb. 1993;13:687-695
9. Austin M. A., Talmud P. J., Luong L. A., Haddad L., Day I. N., Newman B., Edwards K. L., Krauss R. M., Humphries S. E. Candidate-gene studies of the atherogenic lipoprotein phenotype: a sib-pair linkage analysis of DZ women twins. Am. J. Hum. Genet. 1998;62:406-419[Medline]
10.
Campos H., Arnold K. S., Balestra M. E., Innerarity T. L., Krauss R. M. Differences in receptor binding of LDL subfractions. Arterioscler. Thromb. Vasc. Biol. 1996;16:794-801
11.
Campos H., Blijlevens E., McNamara J. R., Ordovas J. M., Posner B. M., Wilson P. W., Castelli W. P., Schaefer E. J. LDL particle size distribution. Results from the Framingham Offspring Study. Arterioscler. Thromb. 1992;12:1410-1419
12. Dreon D. M., Fernstrom H. A., Miller B., Krauss R. M. Low-density lipoprotein subclass patterns and lipoprotein response to a reduced-fat diet in men. FASEB J 1994;8:121-126[Abstract]
13.
Dreon D. M., Fernstrom H. A., Williams P. T., Krauss R. M. A very low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins [see comments]. Am. J. Clin. Nutr. 1999;69:411-418
14.
Dreon D. M., Fernstrom H. A., Williams P. T., Krauss R. M. LDL subclass patterns and lipoprotein response to a low-fat, high-carbohydrate diet in women. Arterioscler. Thromb. Vasc. Biol. 1997;17:707-714
15.
Dreon D. M., Fernstrom H. A., Williams P. T., Krauss R. M. Reduced LDL particle size in children consuming a very-low-fat diet is related to parental LDL-subclass patterns [In Process Citation]. Am. J. Clin. Nutr. 2000;71:1611-1616
16. Dreon D. M., Krauss R. M. Low density lipoprotein subclass patterns are associated with differing lipoprotein responses to low-fat and high-monounsaturated fat diets. Circulation 1995;92(suppl):I-155
17. Dreon D. M., Krauss R. M. Diet-gene interactions in human lipoprotein metabolism. J. Am. Coll. Nutr. 1997;16:313-324[Abstract]
18. Gardner C. D., Fortmann S. P., Krauss R. M. Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women [see comments]. J. Am. Med. Assoc. 1996;276:875-881[Abstract]
19.
Hegsted D. M., Ausman L. M., Johnson J. A., Dallal G. E. Dietary fat and serum lipids: an evaluation of the experimental data [published erratum appears in Am. J. Clin. Nutr. 58: 245]. Am. J. Clin. Nutr. 1993;57:875-883
20.
Katan M. B., Beynen A. C. Characteristics of human hypo- and hyperresponders to dietary cholesterol. Am. J. Epidemiol. 1987;125:387-399
21. Keys A., Anderson J. T., Grande F. Prediction of serum cholesterol responses of man to changes in fats in the diet. Lancet 1957;2:959-966
22. Krauss R. M. Genetic, metabolic, and dietary influences on the atherogenic lipoprotein phenotype. World Rev. Nutr. Diet. 1997;80:22-43[Medline]
23.
Krauss R. M. Genetic recipes for heart-healthy diets [editorial; comment]. Am. J. Clin. Nutr. 2000;71:668-669
24. Krauss R. M., Cantor R. M., Holl L. G., Blanche P. J., Rithaporn T., Rawlings R. S., Fernstrom H. S., Orr J. R., Dreon D. M., Davis R. C., Lusis A. J., Rotter J. I. Linkage of LDL subclass phenotypes to the LDL receptor gene locus on high-fat and low-fat diets. Circulation 1999;100(suppl.):I-659
25.
Krauss R. M., Eckel R. H., Howard B., Appel L. J., Daniels S. R., Deckelbaum R. J., Erdman J. W., Jr., Kris-Etherton P., Goldberg I. J., Kotchen T. A., Lichtenstein A. H., Mitch W. E., Mullis R., Robinson K., Wylie-Rosett J., St. Jeor S., Suttie J., Tribble D. L., Bazzarre T. L. AHA dietary guidelines. Revisions 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation 2000;102(suppl.):2284-2299
26.
Krauss R. M., Dreon D. M. Low-density-lipoprotein subclasses and response to a low-fat diet in healthy men. Am. J. Clin. Nutr. 1995;62:478S-487S
27.
Krauss R. M., Williams P. T., Lindgren F. T., Wood P. D. Coordinate changes in levels of human serum low and high density lipoprotein subclasses in healthy men. Arteriosclerosis 1988;8:155-162
28.
Lamarche B., Tchernof A., Moorjani S., Cantin B., Dagenais G. R., Lupien P. J., Despres J. P. Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Quebec Cardiovascular Study [see comments]. Circulation 1997;95:69-75
29. Lamon-Fava S., Jimenez D., Christian J. C., Fabsitz R. R., Reed T., Carmelli D., Castelli W. P., Ordovas J. M., Wilson P. W., Schaefer E. J. The NHLBI Twin Study: heritability of apolipoprotein A-I, B, and low density lipoprotein subclasses and concordance for lipoprotein(a). Atherosclerosis 1991;91:97-106[Medline]
30.
McNamara J. R., Campos H., Ordovas J. M., Peterson J., Wilson P. W., Schaefer E. J. Effect of gender, age, and lipid status on low density lipoprotein subfraction distribution. Results from the Framingham Offspring Study. Arteriosclerosis 1987;7:483-490
31. Naggert J. K., Recinos A., III, Lamerdin J. E., Krauss R. M., Nishina P. M. The atherogenic lipoprotein phenotype is not caused by a mutation in the coding region of the low density lipoprotein receptor gene. Clin. Genet. 1997;51:236-240[Medline]
32. Nielsen L. B. Transfer of low density lipoprotein into the arterial wall and risk of atherosclerosis. Atherosclerosis 1996;123:1-15[Medline]
33.
Nishina P. M., Johnson J. P., Naggert J. K., Krauss R. M. Linkage of atherogenic lipoprotein phenotype to the low density lipoprotein receptor locus on the short arm of chromosome 19. Proc. Natl. Acad. Sci. U.S.A. 1992;89:708-712
34. Ordovas J. M. The genetics of serum lipid responsiveness to dietary interventions. Proc. Nutr. Soc. 1999;58:171-187[Medline]
35. Reaven G. M., Chen Y. D., Jeppesen J., Maheux P., Krauss R. M. Insulin resistance and hyperinsulinemia in individuals with small, dense low density lipoprotein particles [see comments]. J. Clin. Investig. 1993;92:141-146
36. Rotter J. I., Bu X., Cantor R. M., Warden C. H., Brown J., Gray R. J., Blanche P. J., Krauss R. M., Lusis A. J. Multilocus genetic determinants of LDL particle size in coronary artery disease families. Am. J. Hum. Genet. 1996;58:585-594[Medline]
37.
Schaefer E. J., Lamon-Fava S., Ausman L. M., Ordovas J. M., Clevidence B. A., Judd J. T., Goldin B. R., Woods M., Gorbach S., Lichtenstein A. H. Individual variability in lipoprotein cholesterol response to National Cholesterol Education Program Step 2 diets [see comments]. Am. J. Clin. Nutr. 1997;65:823-830
38. Simopoulos A. P. Genetic variation and nutrition. Nutr. Rev. 1999;57:S10-S19[Medline]
39. Stampfer M. J., Krauss R. M., Ma J., Blanche P. J., Holl L. G., Sacks F. M., Hennekens C. H. A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction [see comments]. J. Am. Med. Assoc. 1996;276:882-888[Abstract]
40.
Talmud P. J., Edwards K. L., Turner C. M., Newman B., Palmen J. M., Humphries S. E., Austin M. A. Linkage of the cholesteryl ester transfer protein (CETP) gene to LDL particle size: use of a novel tetranucleotide repeat within the CETP promoter [In Process Citation]. Circulation 2000;101:2461-2466
41. Terry R. B., Wood P. D., Haskell W. L., Stefanick M. L., Krauss R. M. Regional adiposity patterns in relation to lipids, lipoprotein cholesterol, and lipoprotein subfraction mass in men. J. Clin. Endocrinol. Metab. 1989;68:191-199[Abstract]
42. Tribble D. L., Holl L. G., Wood P. D., Krauss R. M. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189-199[Medline]
This article has been cited by other articles:
|
|
 |
|
  S. Shrestha, H. C. Freake, M. M. McGrane, J. S. Volek, and M. L. Fernandez A Combination of Psyllium and Plant Sterols Alters Lipoprotein Metabolism in Hypercholesterolemic Subjects by Modifying the Intravascular Processing of Lipoproteins and Increasing LDL Uptake J. Nutr., May 1, 2007; 137(5): 1165 - 1170. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Ensign, N. Hill, and C. B. Heward Disparate LDL Phenotypic Classification among 4 Different Methods Assessing LDL Particle Characteristics Clin. Chem., September 1, 2006; 52(9): 1722 - 1727. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Gazi, E. S. Lourida, T. Filippatos, V. Tsimihodimos, M. Elisaf, and A. D. Tselepis Lipoprotein-Associated Phospholipase A2 Activity Is a Marker of Small, Dense LDL Particles in Human Plasma Clin. Chem., December 1, 2005; 51(12): 2264 - 2273. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. S. Bloch Low Carbohydrate Diets, Pro: Time to Rethink Our Current Strategies Nutr Clin Pract, February 1, 2005; 20(1): 3 - 12. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. D. Proctor, D. F. Vine, and J. C.L. Mamo Arterial Permeability and Efflux of Apolipoprotein B-Containing Lipoproteins Assessed by In Situ Perfusion and Three-Dimensional Quantitative Confocal Microscopy Arterioscler. Thromb. Vasc. Biol., November 1, 2004; 24(11): 2162 - 2167. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. N. Ballesteros, R. M. Cabrera, M. del Socorro Saucedo, and M. L. Fernandez Dietary cholesterol does not increase biomarkers for chronic disease in a pediatric population from northern Mexico Am. J. Clinical Nutrition, October 1, 2004; 80(4): 855 - 861. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. L. Herron and M. L. Fernandez Are the Current Dietary Guidelines Regarding Egg Consumption Appropriate? J. Nutr., January 1, 2004; 134(1): 187 - 190. [Full Text] [PDF]
|
|
|
|
|
|
E. Ros Dietary cis-monounsaturated fatty acids and metabolic control in type 2 diabetes Am. J. Clinical Nutrition, September 1, 2003; 78(3): 617S - 625. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. P Mensink, P. L Zock, A. D. Kester, and M. B Katan Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials Am. J. Clinical Nutrition, May 1, 2003; 77(5): 1146 - 1155. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. L. Herron, S. Vega-Lopez, K. Conde, T. Ramjiganesh, N. S. Shachter, and M. L. Fernandez Men Classified as Hypo- or Hyperresponders to Dietary Cholesterol Feeding Exhibit Differences in Lipoprotein Metabolism J. Nutr., April 1, 2003; 133(4): 1036 - 1042. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Sharman, W. J. Kraemer, D. M. Love, N. G. Avery, A. L. Gomez, T. P. Scheett, and J. S. Volek A Ketogenic Diet Favorably Affects Serum Biomarkers for Cardiovascular Disease in Normal-Weight Men J. Nutr., July 1, 2002; 132(7): 1879 - 1885. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
