Metabolism of triglyceride-rich lipoproteins during alimentary lipemia

F Karpe, G Steiner, T Olivecrona, L A Carlson, A Hamsten, F Karpe, G Steiner, T Olivecrona, L A Carlson, A Hamsten

Abstract

The metabolism of chylomicron remnants and VLDL was studied in healthy controls and normo- (NTG) and hypertriglyceridemic (HTG) patients with coronary artery disease after intake of an oral fat load. Specific determination of apo B-48 and B-100 enabled separation of the respective contribution of the two lipoprotein species. The postprandial plasma levels of small (Sf 20-60) and large (Sf 60-400) chylomicron remnants increased in controls and NTG patients. In contrast, only large chylomicron remnants increased in the HTG patients. An increase of large VLDL was seen in response to the oral fat load in all groups, whereas small VLDL were either unchanged in the controls and the NTG patients, or decreased in the HTG patient group. The whole plasma concentration of C apolipoproteins was essentially uninfluenced by the oral fat load, whereas the content in large triglyceride-rich lipoproteins paralleled the apo B elevations in controls and NTG patients. An even more prominent increase of apo B in large triglyceride-rich lipoproteins in the HTG group was not accompanied by an increase of C apolipoproteins. These findings indicate that chylomicrons compete with VLDL for removal of triglycerides by lipoprotein lipase and that the postprandial metabolism of triglyceride-rich lipoproteins is severely defective in hypertriglyceridemia.

References

    1. J Clin Invest. 1987 Apr;79(4):1110-9
    1. J Clin Invest. 1980 Mar;65(3):652-8
    1. Atherosclerosis. 1987 May;65(1-2):75-88
    1. J Clin Invest. 1987 Dec;80(6):1571-7
    1. Baillieres Clin Endocrinol Metab. 1987 Aug;1(3):639-66
    1. J Lipid Res. 1988 Jul;29(7):925-36
    1. Scand J Clin Lab Invest. 1989 Feb;49(1):73-81
    1. Nature. 1989 Sep 14;341(6238):162-4
    1. Proc Natl Acad Sci U S A. 1990 Feb;87(3):909-13
    1. J Lipid Res. 1990 Mar;31(3):545-8
    1. J Biol Chem. 1990 Jun 25;265(18):10771-9
    1. J Biol Chem. 1990 Dec 25;265(36):22453-9
    1. J Lipid Res. 1990 Oct;31(10):1761-9
    1. Arterioscler Thromb. 1991 May-Jun;11(3):653-62
    1. Arterioscler Thromb. 1991 May-Jun;11(3):691-703
    1. Atherosclerosis. 1990 Dec;85(2-3):193-202
    1. Nutrition. 1991 Sep-Oct;7(5):355-7
    1. J Lipid Res. 1992 Jun;33(6):915-30
    1. J Biol Chem. 1951 Nov;193(1):265-75
    1. J Lab Clin Med. 1953 Mar;41(3):486-92
    1. J Atheroscler Res. 1963 Jul-Aug;3:334-6
    1. J Clin Invest. 1975 Dec;56(6):1622-34
    1. Am J Med. 1976 Jan;60(1):80-8
    1. Metabolism. 1976 JUL;25(7):777-801
    1. Proc Natl Acad Sci U S A. 1977 Mar;74(3):1245-9
    1. J Clin Invest. 1977 Jul;60(1):171-80
    1. Circulation. 1979 Sep;60(3):473-85
    1. Clin Chim Acta. 1968 Nov;22(3):393-7
    1. J Clin Invest. 1970 Mar;49(3):465-71
    1. J Clin Invest. 1973 Jan;52(1):32-8
    1. J Biol Chem. 1973 Jul 25;248(14):4941-6
    1. J Clin Invest. 1973 Jul;52(7):1578-85
    1. J Clin Pathol Suppl (Assoc Clin Pathol). 1973;5:32-7
    1. Anal Biochem. 1975 May 12;65(1-2):42-9
    1. Proc Natl Acad Sci U S A. 1980 May;77(5):2465-9
    1. J Immunol Methods. 1980;34(3):243-51
    1. Clin Chem. 1981 Jun;27(6):892-5
    1. Biochim Biophys Acta. 1982 Jul 20;712(1):94-102
    1. J Clin Invest. 1984 Aug;74(2):470-82
    1. J Clin Invest. 1984 Dec;74(6):2178-92
    1. J Lipid Res. 1985 May;26(5):556-65
    1. Adv Exp Med Biol. 1985;183:47-71
    1. Metabolism. 1985 Nov;34(11):983-92
    1. Circulation. 1986 Jun;73(6):1097-110
    1. Arteriosclerosis. 1986 May-Jun;6(3):297-304
    1. Acta Med Scand. 1986;219(5):435-47
    1. J Clin Invest. 1986 Nov;78(5):1287-95
    1. J Lipid Res. 1987 Feb;28(2):195-206

Source: PubMed

3
Abonnere