This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints, Permissions and Rights Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by FALKO, J. M. Articles by STEELMAN, R. Search for Related Content PubMed PubMed Citation Articles by FALKO, J. M. Articles by STEELMAN, R.

Effects of Diet on Apoprotein E Levels and on the Apoprotein E Subspecies in Human Plasma Lipoproteins^*

JAMES M. FALKO, GUSTAV SCHONFELD, JOSEPH L. WITZTUM, JANET B. KOLAR, STUART W. WEIDMAN and ROBERT STEELMAN

Lipid Research Center, Washington University School of Medicine St.Louis,Missouri 63110

Address requests for reprints to: Gustav Schonfeld, M.D., Lipid Research Center, Washington University School of Medicine, Box 8046,4566 Scott Avenue, St. Louis, Missouri 63110.

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 assess whether the relative proportions in ApoE (and hence the ApoE- 3 deficiency in type III) are constant in the faceof 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 hafter the ingestion of 150 g 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 a RIA described in this communication, and the ApoE subspecies were quantified by isoelectric focusing. After 7 days of the carbohydrate diet, fasting triglyceride levelsin 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 theextent 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 hypertriglyceridemic patients further suggests that the two dietary perturbations used in these studies do not alter the relative proportions of the various subspecies of ApoE.

^* This work was supported in part by NIH Contract N01-HV-2-2916-L (Lipid Research Clinic Program) and NIH Grant HL-15308. Presented in part at the National Meeting of the American Federation for Clinical Research, Washington, D.C., May 1979.

Supported by NIH Training Grant 1F32-HL-05566-01. Present address: Division of Endocrinology, Department of Medicine, The Ohio State University College of Medicine, Columbus, Ohio 43210.

Supported in part by the American Heart Association, Missouri Affiliate. Present address: La Jolla Lipid Clinic, M-020, University of California, San Diego,La Jolla, California 92093.

Present address: Division of Gastroenterology, Department of Medicine, The University of Tennessee Center for the Health Sciences,951 Court Avenue,Room 335 M, Memphis, Tennessee 38163.

Received August 15, 1979.

This article has been cited by other articles:

				H. Hidaka, M. Tozuka, E. Hidaka, K. Yamauchi, H. Ota, T. Honda, and T. Katsuyama Characterization of an Apolipoprotein E3 Variant (Arg 145 -> His) Associated with Mild Hypertriglyceridemia Ann. Clin. Lab. Sci., April 1, 2001; 31(2): 163 - 170. [Abstract] [Full Text] [PDF]

				J. S. Cohn, C. Marcoux, and J. Davignon Detection, Quantification, and Characterization of Potentially Atherogenic Triglyceride-Rich Remnant Lipoproteins Arterioscler Thromb Vasc Biol, October 1, 1999; 19(10): 2474 - 2486. [Abstract] [Full Text] [PDF]

				J. S. Cohn, M. Tremblay, M. Amiot, D. Bouthillier, M. Roy, J. Genest Jr, and J. Davignon Plasma Concentration of Apolipoprotein E in Intermediate-Sized Remnant-Like Lipoproteins in Normolipidemic and Hyperlipidemic Subjects Arterioscler Thromb Vasc Biol, January 1, 1996; 16(1): 149 - 159. [Abstract] [Full Text]

				H. B. BREWER Jr., L. A. ZECH, R. E. GREGG, D. SCHWARTZ, and E. J. SCHAEFER Type III Hyperlipoproteinemia: Diagnosis, Molecular Defects, Pathology, and Treatment Ann Intern Med, May 1, 1983; 98(5_Part_1): 623 - 640. [Abstract] [PDF]