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Hypertriglyceridaemia secondary to liver disease

MPG-Autoren
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Müller,  P.
Department of Molecular Developmental Biology, MPI for biophysical chemistry, Max Planck Society;

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Agostini,  Bruno
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Wieland,  Heike
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Seidel,  D.
Max Planck Institute for Medical Research, Max Planck Society;

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Zitation

Müller, P., Fellin, R., Lambrecht, J., Agostini, B., Wieland, H., Rost, W., et al. (1974). Hypertriglyceridaemia secondary to liver disease. European Journal of Clinical Investigation, 4(6), 419-428. doi:10.1111/j.1365-2362.1974.tb02357.x.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002D-FABB-D
Zusammenfassung
Abstract. Some patients with liver dysfunction show a marked hypertriglyceridaemia, a phenomenon most frequently accompanied by cholestasis.

In this report we have identified, isolated and characterized an abnormally large (300–700 Å), triglyceride rich, low density lipoprotein, (d 1.019-1.063 g/ml) designated β-lipoprotein (β2-LP), from the plasma of patients with hypertriglyceridaemia secondary to liver disease. The βa-LP differs significantly in its percent composition and protein moiety from the unique lipoprotein-X (LP-X) specific for cholestasis and also from normal β-lipoproteins, both of which are also present in the patients LDL fraction. Furthermore, some evidence is provided suggesting that the β2-LP is likely to represent an intermediate particle of chylomicron metabolism, which accumulates in this disease due to a markedly diminished hepatic lipase activity.