ArticleMetabolic brain disease2010
Brain energy metabolism parameters in an animal model of diabetes.
Article in Metabolic brain disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- NMR-based metabolomics characterizes metabolic changes in different brain regions of streptozotocin-induced diabetic mice with cognitive decline.Metabolic brain disease · 2020Article
- Diabetes-induced abnormalities of mitochondrial function in rat brain cortex: the effect of n-3 fatty acid diet.Molecular and cellular biochemistry · 2017Article
- Avocado Oil Improves Mitochondrial Function and Decreases Oxidative Stress in Brain of Diabetic Rats.Journal of diabetes research · 2015Article
- Increased oxidative stress and imbalance in antioxidant enzymes in the brains of alloxan-induced diabetic rats.Experimental diabetes research · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of evidence has indicated that altered mitochondrial function may be involved in mechanism for the development of diabetic complications. Thus, we investigated whether animal model of diabetes induced by alloxan alters energy metabolism parameters. Wistar rats received one single injection of alloxan (250 mg/kg) and after 15 days we evaluated mitochondrial respiratory chain complexes I, II, II-III and IV, creatine kinase and citrate synthase activities in prefrontal cortex, hippocampus and striatum. We observed that animal model of diabetes induced by alloxan increased complexes I and IV activities in hippocampus, complexes II and II-III activities in prefrontal cortex and striatum and complex IV in prefrontal cortex; however decreased complex IV activity in striatum. Moreover, diabetes rats decreased creatine kinase activity in striatum and increased citrate synthase activity in hippocampus. In conclusion, this study indicates that the alteration in mitochondrial function is probably involved in the pathophysiology of diabetes.
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