Breakers of advanced glycation end products restore large artery properties in experimental diabetes
Autor: | Sara Vasan, Francy R. L. Crijns, Pierre Poitevin, John J. Egan, Chantal M. Boulanger, Anthony Cerami, Bernard I. Levy, Maya S. P. Huijberts, Geertje N. M. Swennen, Bruce H. R. Wolffenbuttel, Peter C. Ulrich |
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Přispěvatelé: | Interne Geneeskunde, RS: NUTRIM School of Nutrition and Translational Research in Metabolism |
Jazyk: | angličtina |
Rok vydání: | 1998 |
Předmět: |
Glycation End Products
Advanced Male medicine.medical_specialty Carotid Artery Common Connective tissue Blood Pressure macromolecular substances In Vitro Techniques Matrix (biology) Alagebrium Muscle Smooth Vascular Diabetes Mellitus Experimental Heart Rate Glycation Diabetes mellitus Internal medicine medicine Animals Cardiac Output Rats Wistar Multidisciplinary Chemistry Hemodynamics technology industry and agriculture Biological Sciences medicine.disease Rats Compliance (physiology) Thiazoles Cross-Linking Reagents Blood pressure Endocrinology medicine.anatomical_structure Arterial stiffness Collagen Blood Flow Velocity medicine.drug |
Zdroj: | Proceedings of the National Academy of Sciences of the United States of America, 95(8), 4630-4634. National Academy of Sciences |
ISSN: | 0027-8424 |
DOI: | 10.1073/pnas.95.8.4630 |
Popis: | Department of Endocrinology, Cardiovascular Research Institute Maastricht and University (Hospital) Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands.Glucose and other reducing sugars react with proteins by a nonenzymatic, posttranslational modification process called nonenzymatic glycation. The formation of advanced glycation end products (AGEs) on connective tissue and matrix components accounts largely for the increase in collagen crosslinking that accompanies normal aging and which occurs at an accelerated rate in diabetes, leading to an increase in arterial stiffness. A new class of AGE crosslink "breakers" reacts with and cleaves these covalent, AGE-derived protein crosslinks. Treatment of rats with streptozotocin-induced diabetes with the AGE-breaker ALT-711 for 1-3 weeks reversed the diabetes-induced increase of large artery stiffness as measured by systemic arterial compliance, aortic impedance, and carotid artery compliance and distensibility. These findings will have considerable implications for the treatment of patients with diabetes-related complications and aging. |
Databáze: | OpenAIRE |
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