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    Obesity and hepatosteatosis in mice with enhanced oxidative DNA damage processing in mitochondria.

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    Authors
    Zhang, H
    Xie, C
    Spencer, H
    Zuo, C
    Higuchi, M
    Ranganathan, G
    Kern, P
    Chou, M
    Huang, Q
    Szczesny, B
    Mitra, S
    Watson, A
    Margison, Geoffrey P
    Fan, C
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    Affiliation
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
    Issue Date
    2011-04
    
    Metadata
    Show full item record
    Abstract
    Mitochondria play critical roles in oxidative phosphorylation and energy metabolism. Increasing evidence supports that mitochondrial DNA (mtDNA) damage and dysfunction play vital roles in the development of many mitochondria-related diseases, such as obesity, diabetes mellitus, infertility, neurodegenerative disorders, and malignant tumors in humans. Human 8-oxoguanine-DNA glycosylase 1 (hOGG1) transgenic (TG) mice were produced by nuclear microinjection. Transgene integration was analyzed by PCR. Transgene expression was measured by RT-PCR and Western blot analysis. Mitochondrial DNA damage was analyzed by mutational analyses and measurement of mtDNA copy number. Total fat content was measured by a whole-body scan using dual-energy X-ray absorptiometry. The hOGG1 overexpression in mitochondria increased the abundance of intracellular free radicals and major deletions in mtDNA. Obesity in hOGG1 TG mice resulted from increased fat content in tissues, produced by hyperphagia. The molecular mechanisms of obesity involved overexpression of genes in the central orexigenic (appetite-stimulating) pathway, peripheral lipogenesis, down-regulation of genes in the central anorexigenic (appetite-suppressing) pathway, peripheral adaptive thermogenesis, and fatty acid oxidation. Diffuse hepatosteatosis, female infertility, and increased frequency of malignant lymphoma were also seen in these hOGG1 TG mice. High levels of hOGG1 expression in mitochondria, resulting in enhanced oxidative DNA damage processing, may be an important factor in human metabolic syndrome, infertility, and malignancy.
    Citation
    Obesity and hepatosteatosis in mice with enhanced oxidative DNA damage processing in mitochondria. 2011, 178 (4):1715-27 Am J Pathol
    Journal
    American Journal of Pathology
    URI
    http://hdl.handle.net/10541/226738
    DOI
    10.1016/j.ajpath.2010.12.038
    PubMed ID
    21435453
    Type
    Article
    Language
    en
    ISSN
    1525-2191
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.ajpath.2010.12.038
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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