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Diabetes 52:1449-1456, 2003
© 2003 by the American Diabetes Association, Inc.

Increased Vulnerability of Brain Mitochondria in Diabetic (Goto-Kakizaki) Rats With Aging and Amyloid-ß Exposure

Paula I. Moreira1, Maria S. Santos1, António M. Moreno1, Raquel Seiça2, and Catarina R. Oliveira2

1 Center for Neuroscience of Coimbra, Department of Zoology, University of Coimbra, Coimbra, Portugal
2 Faculty of Medicine, University of Coimbra, Coimbra, Portugal

This study evaluated the respiratory indexes (respiratory control ratio [RCR] and ADP/O ratio), mitochondrial transmembrane potential ({Delta}{Psi}m), repolarization lag phase, repolarization level, ATP/ADP ratio, and induction of the permeability transition pore of brain mitochondria isolated from normal Wistar and GK diabetic rats of different ages (1.5, 12, and 24 months of age). The effect of amyloid ß-peptides, 50 µmol/l Aß25–35 or 2 µmol/l Aß1–40, on mitochondrial function was also analyzed. Aging of diabetic mice induced a decrease in brain mitochondrial RCR, ADP/O, and ATP/ADP ratios but induced an increase in the repolarization lag phase. Brain mitochondria from older diabetic rats were more prone to the induction of the permeability transition pore, i.e., mitochondria from 24-month-old diabetic rats accumulated much less Ca2+ (20 µmol/l) than those isolated from 12-month-old rats (50 µmol/l) or 1.5-month-old rats (100 µmol/l). In the presence of 50 µmol/l Aß25–35 or 2 µmol/l Aß1–40, age-related mitochondrial effects were potentiated. These results indicate that diabetes-related mitochondrial dysfunction is exacerbated by aging and/or by the presence of neurotoxic agents such as amyloid ß-peptides, supporting the idea that diabetes and aging are risk factors for the neurodegeneration induced by these peptides.


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