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

Kyu Sang Park, Kyung Jay Nam, Jun Woo Kim, Youn Bok Lee, Chang Yeop Han, June Key Jeong, Hong Kyu Lee, Youngmi Kim Pak

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58 Citations (Scopus)


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 ρ0 SK-Hep1 human hepatoma cells, whose mtDNA was depleted by long-term exposure to ethidium bromide. The ρ0 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 ρ0 cells compared with parental ρ+ 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.

Original languageEnglish
Pages (from-to)E1007-E1014
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number6 43-6
Publication statusPublished - 2001

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)


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