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1 Division of Metabolic Disease, Department of Biomedical Sciences, National Institute of Health, Seoul 122-701; and Departments of 2 Nuclear Medicine and 3 Internal Medicine, School of Medicine, Seoul National University, Seoul 110-744, Korea
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
0 SK-Hep1 human hepatoma cells, whose mtDNA was
depleted by long-term exposure to ethidium bromide. The
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
0 cells compared with parental
+ 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.
oxidative phosphorylation; glucose uptake
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