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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2001-5-14
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pubmed:abstractText |
Maternally inherited mitochondrial DNA (mtDNA) has been suggested to be a genetic factor for diabetes. Reports have shown a decrease of mtDNA content in tissues of diabetic patients. We investigated the effects of mtDNA depletion on glucose metabolism by use of rho(0) SK-Hep1 human hepatoma cells, whose mtDNA was depleted by long-term exposure to ethidium bromide. The rho(0) cells failed to hyperpolarize mitochondrial membrane potential in response to glucose stimulation. Intracellular ATP content, glucose-stimulated ATP production, glucose uptake, steady-state mRNA and protein levels of glucose transporters, and cellular activities of glucose-metabolizing enzymes were decreased in rho(0) cells compared with parental rho(+) cells. Our results suggest that the quantitative reduction of mtDNA may suppress the expression of nuclear DNA-encoded glucose transporters and enzymes of glucose metabolism. Thus this may lead to diabetic status, such as decreased ATP production and glucose utilization.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Mitochondrial,
http://linkedlifedata.com/resource/pubmed/chemical/Electron Transport Complex IV,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Ethidium,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Glucosephosphate Dehydrogenase,
http://linkedlifedata.com/resource/pubmed/chemical/Glyceraldehyde-3-Phosphate...,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoglycemic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Monosaccharide Transport Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0193-1849
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
280
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E1007-14
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11350783-Adenosine Triphosphate,
pubmed-meshheading:11350783-Carcinoma, Hepatocellular,
pubmed-meshheading:11350783-DNA, Mitochondrial,
pubmed-meshheading:11350783-Diabetes Mellitus, Type 1,
pubmed-meshheading:11350783-Electron Transport Complex IV,
pubmed-meshheading:11350783-Enzyme Inhibitors,
pubmed-meshheading:11350783-Ethidium,
pubmed-meshheading:11350783-Glucose,
pubmed-meshheading:11350783-Glucosephosphate Dehydrogenase,
pubmed-meshheading:11350783-Glyceraldehyde-3-Phosphate Dehydrogenases,
pubmed-meshheading:11350783-Humans,
pubmed-meshheading:11350783-Hypoglycemic Agents,
pubmed-meshheading:11350783-Insulin,
pubmed-meshheading:11350783-Liver Neoplasms,
pubmed-meshheading:11350783-Mitochondria,
pubmed-meshheading:11350783-Monosaccharide Transport Proteins,
pubmed-meshheading:11350783-Oxidative Phosphorylation,
pubmed-meshheading:11350783-Tumor Cells, Cultured
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pubmed:year |
2001
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pubmed:articleTitle |
Depletion of mitochondrial DNA alters glucose metabolism in SK-Hep1 cells.
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pubmed:affiliation |
Division of Metabolic Disease, Department of Biomedical Sciences, National Institute of Health, Seoul 122-701, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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