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Am J Physiol Endocrinol Metab 280: E1007-E1014, 2001;
0193-1849/01 $5.00
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Vol. 280, Issue 6, E1007-E1014, June 2001

Depletion of mitochondrial DNA alters glucose metabolism in SK-Hep1 cells

Kyu-Sang Park1, Kyung-Jay Nam1, Jun-Woo Kim1, Youn-Bok Lee1, Chang-Yeop Han1, June-Key Jeong2, Hong-Kyu Lee1,3, and Youngmi Kim Pak1

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 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.

oxidative phosphorylation; glucose uptake


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