Cited by 117Mitochondrial Function and PathologyAlzheimer's disease research and treatmentsAutophagy in Disease and Therapy

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

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Moreira, Paula I., Santos, Maria S., Moreno, António M., Seiça, Raquel, Oliveira, Catarina R.·2003·Diabetes

DOI 10.2337/diabetes.52.6.1449

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Abstract

This study evaluated the respiratory indexes (respiratory control ratio [RCR] and ADP/O ratio), mitochondrial transmembrane potential (ΔΨm), 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 β-peptides, 50 μmol/l Aβ25–35 or 2 μmol/l Aβ1–40, 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 Aβ25–35 or 2 μmol/l Aβ1–40, 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 β-peptides, supporting the idea that diabetes and aging are risk factors for the neurodegeneration induced by these peptides.

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Authors: Moreira, P. I., Santos, M. S., Moreno, A. M., Seiça, R., & Oliveira, C. R.
Affiliations: University of Coimbra (PT)
Center for Neuroscience of Coimbra, Department of Zoology, University of Coimbra, Coimbra, Portugal
Faculty of Medicine, University of Coimbra, Coimbra, Portugal
ORCID: Moreira, Paula I.
Santos, Maria S.
Oliveira, Catarina R.
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2003-06-01
Volume: 52
Issue: 6
Pages: 1449-1456
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/diabetes.52.6.1449
OpenAlex: W2119876958
Cited by: 117
References: 54
Citations by year: 2026: 1 · 2025: 3 · 2024: 7 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 1 · 2019: 7 · 2018: 8 · 2017: 9 · 2016: 7 · 2015: 6 · 2014: 4 · 2013: 7 · 2012: 9
FWCI: 2.19
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Diabetes (publishedVersion)
PubMed (publishedVersion)
Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, other-oa)
Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion)
Funders: Fundação para a Ciência e a Tecnologia
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords: brain mitochondria, mitochondrial dysfunction, aging, amyloid-beta, Goto-Kakizaki rats, mitochondrial permeability transition pore, mitochondrial membrane potential, respiratory control ratio, ADP/O ratio, ATP/ADP ratio, calcium accumulation, neurodegeneration, Alzheimer's disease
MeSH terms: Adenine Nucleotides, Aging, Animals, Brain, Diabetes Mellitus, Type 2, Glycated Hemoglobin, Membrane Potentials, Mitochondria, Oxygen Consumption, Rats, Mutant Strains, Reference Values, Amyloid beta-Peptides, Rats, Wistar, Rats

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

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