Structural and compositional modifications of diabetic low‐density lipoproteins influence their receptor‐mediated uptake by hepatocytes
| Autor: | M Königer, M. W. Baumstark, Peter Schollmeyer, T Quaschning, Christoph Wanner, A. Krämer-Guth, Winfried März, M. Nauck, J. Galle |
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| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Glycosylation Apolipoprotein B Arteriosclerosis Protein Conformation Clinical Biochemistry Biological Transport Active Biochemistry Cell Line Pathogenesis Glycation In vivo Internal medicine Diabetes mellitus medicine Humans Acetic Acid Aged biology Chemistry General Medicine Receptor-mediated endocytosis Middle Aged medicine.disease Pathophysiology Lipoproteins LDL Sterols Endocrinology Diabetes Mellitus Type 2 Liver Receptors LDL LDL receptor biology.protein Female lipids (amino acids peptides and proteins) Cholesterol Esters Oxidation-Reduction Diabetic Angiopathies Oleic Acid |
| Zdroj: | European Journal of Clinical Investigation. 27:460-468 |
| ISSN: | 1365-2362 0014-2972 |
| Popis: | Dyslipoproteinaemia is an important risk factor for the development of atherosclerosis in non-insulin-dependent diabetes mellitus (NIDDM). This study shows that the uptake of low-density lipoproteins (LDLs) prepared from the plasma of patients with NIDDM in cultured human hepatoma cells is largely reduced. In addition, diabetic LDL was less effective in suppressing intracellular cholesterol synthesis. This is because of physicochemical and biochemical differences between lipoproteins from diabetic and from normal individuals. LDL from patients with NIDDM was abnormal with regard to charge, the degree of glycation, the lipid composition and the conformation of the apolipoprotein B receptor-binding domain. The diminished receptor-mediated uptake of apolipoprotein B-containing lipoproteins in diabetic individuals most probably leads to the accumulation of these lipoproteins in vivo and may be of great importance to the pathogenesis of atheroclerosis in these patients. |
| Databáze: | OpenAIRE |
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