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KMID : 0667720000370000415
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Report Natlonal Institute of Health
2000 Volume.37 No. 0 p.415 ~ p.416
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Depletion of mitochondrial DNA alters glucose metabolism in SK-Hep1 cells
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박규상/Park, K. S.
남경재/김준우/이연복/한창엽/정준기/이홍규/Nam, K. J./Kim, J. W./Lee, Y. B./Han, C. Y./Jeong, J. K./Lee, H. K.
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Abstract
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Purpose : Maternally inherited mitochondrial DNA (mtDNA) has been suggested to be a genetic faCtor for diabetes. Reports have shown a decrease of mtDNA contents in tissues of diabetic patients.
Methods: We investigated the effects of mtDNA depletion on glucose metabolism using ρ^(o) SK-Hepl human hepatoma cells, whose mtDNA were depleted by long-term exposure to ethidium bromide.
Results : The ρ^(o) cells failed to hyperpolarize mitochondrial membrane potential in response to glucose stimulation. The 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 ρ^(o) cells when compared to the parental ρ^(+) cells.
Conclusions : Our results suggested 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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KEYWORD
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