| Diabetes and mitochondrial bioenergetics: alterations with age. | |
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MedLine Citation:
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PMID: 12898645 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Several studies have been carried out to evaluate the alterations in mitochondrial functions of diabetic rats. However, some of the results reported are controversial, since experimental conditions, such as aging, and/or strain of animals used were different. The purpose of this study was to evaluate the metabolic changes in liver mitochondria, both in the presence of severe hyperglycaemia (STZ-treated rats) and mild hyperglycaemia (Goto-Kakizaki (GK) rats). Moreover, metabolic alterations were evaluated both at initial and at advanced states of the disease. We observed that both models of type 1 and type 2 diabetes presented alterations on respiratory chain activity. Because of continual severe hyperglycaemia, 9 weeks after the induction of diabetes, the respiratory function declined in STZ-treated rats, as observed by membrane potential and respiratory ratios (RCR, P/O, and FCCP-stimulated respiration) assessment. In contrast, GK rats of 6 months age presented increased respiratory ratios. To localize which respiratory complexes are affected by diabetes, enzymatic respiratory chain activities were evaluated. We observed that succinate dehydrogenase and cytochrome c oxidase activities were significantly augmented both in STZ-treated rats and GK rats of 6 months age. Moreover, H(+)-ATPase activity was also significantly increased in STZ-treated rats with 3 weeks of diabetes and in GK rats of 6 months age as compared to controls. Therefore, these results clearly suggest that both animal models of diabetes present some metabolic adjustments in order to circumvent the deleterious effects promoted by the high glucose levels typical of the disease. |
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Authors:
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Fernanda M Ferreira; Carlos M Palmeira; Raquel Seiça; António J Moreno; Maria S Santos |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of biochemical and molecular toxicology Volume: 17 ISSN: 1095-6670 ISO Abbreviation: J. Biochem. Mol. Toxicol. Publication Date: 2003 |
Date Detail:
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Created Date: 2003-08-04 Completed Date: 2004-03-26 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9717231 Medline TA: J Biochem Mol Toxicol Country: United States |
Other Details:
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Languages: eng Pagination: 214-22 Citation Subset: IM |
Copyright Information:
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Copyright 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:214-222, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10081 |
Affiliation:
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Department of Zoology, Center for Neurosciences and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aging
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metabolism* Animals Body Weight Cell Respiration Diabetes Mellitus / chemically induced, enzymology, metabolism*, pathology* Energy Metabolism* Glycemic Index Mitochondria / enzymology*, metabolism Rats Rats, Inbred Strains Rats, Wistar |
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