Lee 2013 Abstract MiP2013

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Lee HK (2013) Building the mitochondrial medicine; need to define mtDNA variations and its function. Mitochondr Physiol Network 18.08.
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Hong Kyu Lee
MiP2013, Book of Abstracts Open Access

Lee HK (2013)

Event: MiPNet18.08_MiP2013

Mitochondrion is at the center of life phenomena; it supplies energy, controls tasks of the cell, i.e., signaling, differentiation, growth, and death. We found the evidences that mitochondrial dysfunction is causally related to diabetes mellitus, metabolic syndrome and lately atherosclerosis [1,2] and its genome (mtDNA) variations confer a genetic susceptibility to these states [3], we were reconstructing pathogenic mechanisms. We found poor mitochondrial biogenesis during development, be it fetal or after the birth, might be behind so-called thrifty phenotype hypothesis [4], and environmental pollutants could cause those diseases by damaging mitochondrion [5,6]. This scheme could easily explain why diabetes and obesity are associated with enhanced cancer risk.

I reasoned that defining function of different mtDNA should be a cornerstone to build a coherent mitochondrion centered disease model, as mitochondrion is also controlled by nuclear genes. It is better if it is defined quantitatively, as it could be linked to whole body in quantitative terms, applying metabolic scale law. However our efforts were not successful so far. In this presentation, I will explain why comparative mitochondrial physiologic studies are essential.


O2k-Network Lab: KR Seoul Lee HK


Labels: MiParea: mtDNA;mt-genetics, Comparative MiP;environmental MiP, mt-Medicine  Pathology: Cancer, Diabetes, Other 

Organism: Human  Tissue;cell: Other cell lines 



HRR: Theory 

MiP2013 

Affiliations and author contributions

Eulji Medical College and Eulji Hospital, Seoul, South Korea. - Email: hkleemd@eulji.ac.kr

References

  1. Song J, Oh JY, Sung YA, Pak YK, Park KS, Lee HK (2001) Peripheral blood mitochondrial DNA content is related to insulin sensitivity in offspring of type 2 diabetic patients. Diabetes Care 24: 865-869.
  2. Lee HK, Shim EB (2013) Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine-disrupting chemicals and biophysical laws. J Diabetes Investig 4 : 19-33.
  3. Fuku N, Park KS, Yamada Y, Nishigaki Y, Cho YM, Matsuo H, Segawa T, Watanabe S, Kato K, Yokoi K, Nozawa Y, Lee HK, Tanaka M (2007) Mitochondrial haplogroup N9a confers resistance against type 2 diabetes in Asians. Am J Hum Genet 80: 407-415.
  4. Lee HK, Park KS, Cho YM, Lee YY, Pak YK. (2005) Mitochondria-based model for fetal origin of adult disease and insulin resistance. Ann N Y Acad Sci 1042: 1-18.
  5. Lim S, Ahn SY, Song IC, Chung MH, Jang HC, Park KS, Lee KU, Pak YK, Lee HK (2009) Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance. PLoS One 4: e5186.
  6. Park WH, Jun DW, Kim JT, Jeong JH, Park H, Chang YS, Park KS, Lee HK, Pak YK (2013) Novel cell-based assay reveals associations of circulating serum AhR-ligands with metabolic syndrome and mitochondrial dysfunction. Biofactors 30 doi: 10.1002/biof 1092.