Streptozotocin-induced diabetes progressively increases blood-brain barrier permeability in specific brain regions in rats
Autor: | Jason D. Huber, Reyna L. VanGilder, Kimberly A Houser |
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Rok vydání: | 2006 |
Předmět: |
Central Nervous System
Male Sucrose medicine.medical_specialty Physiology medicine.medical_treatment Central nervous system Vascular permeability Tritium Blood–brain barrier Diabetes Mellitus Experimental Tight Junctions Capillary Permeability Rats Sprague-Dawley chemistry.chemical_compound Physiology (medical) Diabetes mellitus Internal medicine medicine Animals Hypoglycemic Agents Insulin Carbon Radioisotopes Coloring Agents Evans Blue business.industry Microcirculation Brain medicine.disease Streptozotocin Rats Disease Models Animal Endocrinology medicine.anatomical_structure chemistry Cerebral blood flow Blood-Brain Barrier Regional Blood Flow Endothelium Vascular Cognition Disorders Cardiology and Cardiovascular Medicine business medicine.drug |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 291:H2660-H2668 |
ISSN: | 1522-1539 0363-6135 |
DOI: | 10.1152/ajpheart.00489.2006 |
Popis: | This study investigated the effects of streptozotocin-induced diabetes on the functional integrity of the blood-brain barrier in the rat at 7, 28, 56, and 90 days, using vascular space markers ranging in size from 342 to 65,000 Da. We also examined the effect of insulin treatment of diabetes on the formation and progression of cerebral microvascular damage and determined whether observed functional changes occurred globally throughout the brain or within specific brain regions. Results demonstrate that streptozotocin-induced diabetes produced a progressive increase in blood-brain barrier permeability to small molecules from 28 to 90 days and these changes in blood-brain barrier permeability were region specific, with the midbrain most susceptible to diabetes-induced microvascular damage. In addition, results showed that insulin treatment of diabetes attenuated blood-brain barrier disruption, especially during the first few weeks; however, as diabetes progressed, it was evident that microvascular damage occurred even when hyperglycemia was controlled. Overall, results of this study suggest that diabetes-induced perturbations to cerebral microvessels may disrupt homeostasis and contribute to long-term cognitive and functional deficits of the central nervous system. |
Databáze: | OpenAIRE |
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