Effects of diet on apoprotein E levels and on the apoprotein E subspecies in human plasma lipoproteins

J. M. Falko, G. Schonfeld, J. Witztum, J. B. Kolar, S. W. Weidman, Robert Steelman

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Type III hyperlipoproteinemia is characterized by a marked deficiency of the apoprotein E (ApoE)-3 subspecies of ApoE in very low density lipoproteins (VLDL). To asses whether the relative proportions in ApoE (and hence the ApoE-3 deficiency in type III) are constant in the face of dietary alterations, we studied seven type III subjects, five subjects with primary endogenous hypertriglyceridemia (type IV), and six normal controls before and after they ate a high carbohydrate diet. In addition, three type III subjects and two normal controls were studied before and 4 h after the ingestion of 150g of a corn oil emulsion. Lipids were measured chemically on lipoprotein fractions isolated by ultracentrifugation and heparin-MnCl2 precipitation. ApoE levels in plasma and VLDL were measured by RIA described in this communication and the ApoE subspecies were quantified by isoelectric focusing. After 7 days of the carbohydrate diet, fasting triglyceride levels in VLDL [density (d) <1.006] rose ~90% over basal levels, and all lipoprotein lipid compositions were altered. ApoE levels in whole plasma remained relatively constant, but ApoE rose in VLDL (d <1.006) and fell in the d > 1.006 infranates. The relative proportions of the ApoE subspecies in VLDL (d <1.006) and in VLDL subfractions (S(f) 20-60, S(f) 60-100, and S(f) 100-400; isolated by density gradient ultracentrifugation) remained unchanged, i.e. ApoE-3 continued to be absent in patients with type III hyperlipidemia, and the proportions of ApoE subspecies remained unchanged in the VLDL of normal controls and hypertriglyceridemic (type IV) subjects. Triglyceride levels rose by ~75% 4 h after the fat meal, but ApoE-3 deficiency persisted in the S(f) > 400 (chylomicron) fractions of type III subjects and the proportion of the ApoE subspecies in chylomicrons of normal controls also remained unchanged. These data suggest that to the extent that the ApoE on VLDL and chylomicrons represented newly secreted ApoE, the ApoE-3 deficiency in type III was already present in newly secreted apoproteins. The constancy of the ApoE patterns in normals and hypertriglycerimidemic patients further suggests that the two dietary perturbations used in these studies do not alter the relative proportions of the various subspecies of ApoE.

Original languageEnglish (US)
Pages (from-to)521-528
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume50
Issue number3
StatePublished - 1980
Externally publishedYes

Fingerprint

Plasma (human)
Apolipoproteins E
Nutrition
Lipoproteins
Diet
VLDL Lipoproteins
Chylomicrons
Hyperlipoproteinemia Type III
Carbohydrates
Apoproteins
Corn Oil
Equidae
Hypertriglyceridemia
Ultracentrifugation
Isoelectric Focusing
Emulsions

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Effects of diet on apoprotein E levels and on the apoprotein E subspecies in human plasma lipoproteins. / Falko, J. M.; Schonfeld, G.; Witztum, J.; Kolar, J. B.; Weidman, S. W.; Steelman, Robert.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 50, No. 3, 1980, p. 521-528.

Research output: Contribution to journalArticle

Falko, J. M. ; Schonfeld, G. ; Witztum, J. ; Kolar, J. B. ; Weidman, S. W. ; Steelman, Robert. / Effects of diet on apoprotein E levels and on the apoprotein E subspecies in human plasma lipoproteins. In: Journal of Clinical Endocrinology and Metabolism. 1980 ; Vol. 50, No. 3. pp. 521-528.
@article{351f21f2482f4037a7e6325a19cdaa2f,
title = "Effects of diet on apoprotein E levels and on the apoprotein E subspecies in human plasma lipoproteins",
abstract = "Type III hyperlipoproteinemia is characterized by a marked deficiency of the apoprotein E (ApoE)-3 subspecies of ApoE in very low density lipoproteins (VLDL). To asses whether the relative proportions in ApoE (and hence the ApoE-3 deficiency in type III) are constant in the face of dietary alterations, we studied seven type III subjects, five subjects with primary endogenous hypertriglyceridemia (type IV), and six normal controls before and after they ate a high carbohydrate diet. In addition, three type III subjects and two normal controls were studied before and 4 h after the ingestion of 150g of a corn oil emulsion. Lipids were measured chemically on lipoprotein fractions isolated by ultracentrifugation and heparin-MnCl2 precipitation. ApoE levels in plasma and VLDL were measured by RIA described in this communication and the ApoE subspecies were quantified by isoelectric focusing. After 7 days of the carbohydrate diet, fasting triglyceride levels in VLDL [density (d) <1.006] rose ~90{\%} over basal levels, and all lipoprotein lipid compositions were altered. ApoE levels in whole plasma remained relatively constant, but ApoE rose in VLDL (d <1.006) and fell in the d > 1.006 infranates. The relative proportions of the ApoE subspecies in VLDL (d <1.006) and in VLDL subfractions (S(f) 20-60, S(f) 60-100, and S(f) 100-400; isolated by density gradient ultracentrifugation) remained unchanged, i.e. ApoE-3 continued to be absent in patients with type III hyperlipidemia, and the proportions of ApoE subspecies remained unchanged in the VLDL of normal controls and hypertriglyceridemic (type IV) subjects. Triglyceride levels rose by ~75{\%} 4 h after the fat meal, but ApoE-3 deficiency persisted in the S(f) > 400 (chylomicron) fractions of type III subjects and the proportion of the ApoE subspecies in chylomicrons of normal controls also remained unchanged. These data suggest that to the extent that the ApoE on VLDL and chylomicrons represented newly secreted ApoE, the ApoE-3 deficiency in type III was already present in newly secreted apoproteins. The constancy of the ApoE patterns in normals and hypertriglycerimidemic patients further suggests that the two dietary perturbations used in these studies do not alter the relative proportions of the various subspecies of ApoE.",
author = "Falko, {J. M.} and G. Schonfeld and J. Witztum and Kolar, {J. B.} and Weidman, {S. W.} and Robert Steelman",
year = "1980",
language = "English (US)",
volume = "50",
pages = "521--528",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "3",

}

TY - JOUR

T1 - Effects of diet on apoprotein E levels and on the apoprotein E subspecies in human plasma lipoproteins

AU - Falko, J. M.

AU - Schonfeld, G.

AU - Witztum, J.

AU - Kolar, J. B.

AU - Weidman, S. W.

AU - Steelman, Robert

PY - 1980

Y1 - 1980

N2 - Type III hyperlipoproteinemia is characterized by a marked deficiency of the apoprotein E (ApoE)-3 subspecies of ApoE in very low density lipoproteins (VLDL). To asses whether the relative proportions in ApoE (and hence the ApoE-3 deficiency in type III) are constant in the face of dietary alterations, we studied seven type III subjects, five subjects with primary endogenous hypertriglyceridemia (type IV), and six normal controls before and after they ate a high carbohydrate diet. In addition, three type III subjects and two normal controls were studied before and 4 h after the ingestion of 150g of a corn oil emulsion. Lipids were measured chemically on lipoprotein fractions isolated by ultracentrifugation and heparin-MnCl2 precipitation. ApoE levels in plasma and VLDL were measured by RIA described in this communication and the ApoE subspecies were quantified by isoelectric focusing. After 7 days of the carbohydrate diet, fasting triglyceride levels in VLDL [density (d) <1.006] rose ~90% over basal levels, and all lipoprotein lipid compositions were altered. ApoE levels in whole plasma remained relatively constant, but ApoE rose in VLDL (d <1.006) and fell in the d > 1.006 infranates. The relative proportions of the ApoE subspecies in VLDL (d <1.006) and in VLDL subfractions (S(f) 20-60, S(f) 60-100, and S(f) 100-400; isolated by density gradient ultracentrifugation) remained unchanged, i.e. ApoE-3 continued to be absent in patients with type III hyperlipidemia, and the proportions of ApoE subspecies remained unchanged in the VLDL of normal controls and hypertriglyceridemic (type IV) subjects. Triglyceride levels rose by ~75% 4 h after the fat meal, but ApoE-3 deficiency persisted in the S(f) > 400 (chylomicron) fractions of type III subjects and the proportion of the ApoE subspecies in chylomicrons of normal controls also remained unchanged. These data suggest that to the extent that the ApoE on VLDL and chylomicrons represented newly secreted ApoE, the ApoE-3 deficiency in type III was already present in newly secreted apoproteins. The constancy of the ApoE patterns in normals and hypertriglycerimidemic patients further suggests that the two dietary perturbations used in these studies do not alter the relative proportions of the various subspecies of ApoE.

AB - Type III hyperlipoproteinemia is characterized by a marked deficiency of the apoprotein E (ApoE)-3 subspecies of ApoE in very low density lipoproteins (VLDL). To asses whether the relative proportions in ApoE (and hence the ApoE-3 deficiency in type III) are constant in the face of dietary alterations, we studied seven type III subjects, five subjects with primary endogenous hypertriglyceridemia (type IV), and six normal controls before and after they ate a high carbohydrate diet. In addition, three type III subjects and two normal controls were studied before and 4 h after the ingestion of 150g of a corn oil emulsion. Lipids were measured chemically on lipoprotein fractions isolated by ultracentrifugation and heparin-MnCl2 precipitation. ApoE levels in plasma and VLDL were measured by RIA described in this communication and the ApoE subspecies were quantified by isoelectric focusing. After 7 days of the carbohydrate diet, fasting triglyceride levels in VLDL [density (d) <1.006] rose ~90% over basal levels, and all lipoprotein lipid compositions were altered. ApoE levels in whole plasma remained relatively constant, but ApoE rose in VLDL (d <1.006) and fell in the d > 1.006 infranates. The relative proportions of the ApoE subspecies in VLDL (d <1.006) and in VLDL subfractions (S(f) 20-60, S(f) 60-100, and S(f) 100-400; isolated by density gradient ultracentrifugation) remained unchanged, i.e. ApoE-3 continued to be absent in patients with type III hyperlipidemia, and the proportions of ApoE subspecies remained unchanged in the VLDL of normal controls and hypertriglyceridemic (type IV) subjects. Triglyceride levels rose by ~75% 4 h after the fat meal, but ApoE-3 deficiency persisted in the S(f) > 400 (chylomicron) fractions of type III subjects and the proportion of the ApoE subspecies in chylomicrons of normal controls also remained unchanged. These data suggest that to the extent that the ApoE on VLDL and chylomicrons represented newly secreted ApoE, the ApoE-3 deficiency in type III was already present in newly secreted apoproteins. The constancy of the ApoE patterns in normals and hypertriglycerimidemic patients further suggests that the two dietary perturbations used in these studies do not alter the relative proportions of the various subspecies of ApoE.

UR - http://www.scopus.com/inward/record.url?scp=0018965486&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018965486&partnerID=8YFLogxK

M3 - Article

C2 - 7358833

AN - SCOPUS:0018965486

VL - 50

SP - 521

EP - 528

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 3

ER -