Adipose tissue lipoprotein lipase activity in type III hyperlipoproteinemia. |
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Authors: | A P Goldberg D M Applebaum-Bowden W R Hazzard |
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Affiliation: | 1. Department of Medicine, Division of Metabolism and Endocrinology, University of Washington, Seattle, Wash. USA;2. the Northwest Lipid Research Clinic, University of Washington, Seattle, Wash. USA |
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Abstract: | An impairment in the catabolism of chylomicron and very low density lipoprotein remnants appears to cause the lipid abnormalities in type III hyperlipoproteinemia. A reduction in the activity of lipoprotein lipase (LPL) has been suggested as the catabolic defect. Results in this study indicate that the activity of adipose tissue LPL measured in the fasted and fed states are in the normal range in type III hyperlipoproteinemia (fasted: type III = 2.7 +/- 1.8 mU/10(6) cells, N = 8; normals = 3.4 +/- 2.5, N = 23, p, not significant; fed: type III = 3.6 +/- 2.1, N = 7; normals = 4.8 +/- 1.8, N = 12, p, not significant). This suggests that perhaps another mechanism, such as the interaction between LPL and its lipid substrate, is abnormal, or that the activity of LPL derived from another tissue source is deficient. |
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Keywords: | Address reprint requests to William R. Hazzard M.D. Northwest Lipid Research Clinic 326 Ninth Avenue Seattle Wash. 98104. |
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