Effect of desialylation of very low-density lipoproteins on their catabolism by lipoprotein lipase
| Autor: | B.A. Hynd, Keijiro Saku, Moti L. Kashyap, A.M. Stoline |
|---|---|
| Rok vydání: | 1985 |
| Předmět: |
Adult
Male medicine.medical_specialty Very low-density lipoprotein Chemical Phenomena Lipolysis Endocrinology Diabetes and Metabolism Neuraminidase In Vitro Techniques Lipoproteins VLDL chemistry.chemical_compound Endocrinology Internal medicine polycyclic compounds medicine Humans Lipoprotein lipase Triglyceride Chemistry Catabolism Hypertriglyceridemia nutritional and metabolic diseases Metabolism Middle Aged medicine.disease N-Acetylneuraminic Acid Sialic acid Lipoprotein Lipase Spectrometry Fluorescence Liver Biochemistry Sialic Acids Female lipids (amino acids peptides and proteins) Isoelectric Focusing |
| Zdroj: | Metabolism. 34:30-35 |
| ISSN: | 0026-0495 |
| DOI: | 10.1016/0026-0495(85)90056-3 |
| Popis: | Very low-density lipoproteins (VLDL) contain sialylated apolipoproteins (apo) (eg, apo CIII1–3) that inhibit apo CII activation of lipoprotein lipase (LPL) and also uptake of triglyceride (TG)-rich lipoproteins by the liver. Hypertriglyceridemic patients can have an excess of sialylated apo CIII (apo CIII1 or apo CIII2) in VLDL. These observations have prompted the notion that sialic acid in VLDL may impede LPL or receptor-mediated clearance of VLDL and thus result in hypertriglyceridemia. The aim of this study was to determine whether desialylation of VLDL altered their property as a substrate for LPL. VLDL isolated from five hypertriglyceridemic patients was desialylated with neuraminidase, labeled with a fluorescent probe, dansyl phosphatidylethanolamine and 600 μg of labeled VLDL TG were incubated with a constant amount of purified bovine LPL.22 The change in fluorescence against time was monitored on a recorder to yield curves representing continuous lipolysis of VLDL by LPL. Mean initial velocity of reaction (Vi) and extent of lipolysis measured as total increase in fluorescence over baseline at 30 minutes ( F30 FO ) were similar (Vi = 10.2 ± 0.37 control v 10.2 ± 0.42 u/min desialylated VLDL; F30 FO = 4.1 ± 0.15, control v 4.1 ± 0.07 desialylated VLDL ; n = 5). Thus, sialic acid does not influence VLDL catabolism by LPL. Our study does not exclude a possible role of the sialic acid in receptor mediated uptake of remnants produced by initial catabolism of VLDL by LPL. |
| Databáze: | OpenAIRE |
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