Difference between revisions of "Lee 2017 MiP2017"
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{{Abstract | {{Abstract | ||
|title=[[Image: | |title=[[Image:LeeHK.jpg|left|90px|Hong Kyu Lee]] Functional difference of mitochondrial genome and its association with phenotypes of metabolic syndrome. | ||
|info=[[MiP2017]] | |info=[[MiP2017]] | ||
|authors=Lee HK, Cho YM, Park KS, Pak YK, Tanaka M | |||
|year=2017 | |year=2017 | ||
|event=MiP2017 | |event=MiP2017 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] Common mitochondrial DNA polymorphisms are susceptibility genome for type 2 diabetes and show functional differences. This fact is well established by generations of conplastic animals, which have the same nuclear genome but different mitochondrial genomes. Animals selected for low aerobic capacity scored high on cardiovascular risk factors that constitute the metabolic syndrome, suggesting mitochondrial function is closely associated with it. However reports examining the functional difference of mitochondrial genome at the cellular level are scarce. We made trans-mitochondrial cytoplasmic hybrid cells (cybrids) with common Asian mtDNA haplogroups A, B, D, and F from young healthy volunteers and analyzed their bioenergetic functions and growth behaviors ''in vitro'' and ''in vivo''. The mitochondrial oxygen consumption rates of cybrids were associated with quantitative parameters of components of metabolic syndrome such as body mass index, waist circumference, serum triglyceride levels and high-density lipoprotein cholesterol levels of donors. In addition, the cybrids showed different growth patterns both ''in vitro'' and ''in vivo'', which were statistically different. Especially, the cybrids harboring mtDNA haplogroup D had a significantly slower growth rate. These findings suggest that mitochondrial genome could be a determinant of phenotypes of common complex diseases. Variations in mitochondrial genome as well as nuclear genome should be considered in explaining the genetic pathogenesis of common complex diseases. | ||
|editor=[[Kandolf G]] | |editor=[[Kandolf G]] | ||
}} | }} | ||
{{Labeling}} | {{Labeling | ||
|area=mtDNA;mt-genetics | |||
|organism=Human | |||
}} | |||
== Affiliations == | == Affiliations == | ||
::::Lee HK(1), Cho YM(2), Park KS(2), Pak YK(3), Tanaka M(4) | |||
::::#Dept Int Med, Univ Eulji | |||
::::#Seoul Nat Univ | |||
::::#Dept Physiol, Kyung Hee Univ, Korea | |||
::::#Dept Clin Lab, Tokyo Metro Geront Hosp, Japan. - [email protected] | |||
== References == | == References == | ||
::::#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 80:407-15. | |||
::::#Hwang S, Kwak SH, Bhak J, Kang HS, Lee YR, Koo BK, Park KS, Lee HK, Cho YM (2011) Gene expression pattern in transmitochondrial cytoplasmic hybrid cells harboring type 2 diabetes-associated mitochondrial DNA haplogroups. PLoS One 6:e22116. | |||
::::#Wallace DC (2015) Mitochondrial DNA variation in human radiation and disease. Cell 163:33-8. | |||
Revision as of 10:31, 13 October 2017
 |
Link: MiP2017
Lee HK, Cho YM, Park KS, Pak YK, Tanaka M (2017)
Event: MiP2017
Common mitochondrial DNA polymorphisms are susceptibility genome for type 2 diabetes and show functional differences. This fact is well established by generations of conplastic animals, which have the same nuclear genome but different mitochondrial genomes. Animals selected for low aerobic capacity scored high on cardiovascular risk factors that constitute the metabolic syndrome, suggesting mitochondrial function is closely associated with it. However reports examining the functional difference of mitochondrial genome at the cellular level are scarce. We made trans-mitochondrial cytoplasmic hybrid cells (cybrids) with common Asian mtDNA haplogroups A, B, D, and F from young healthy volunteers and analyzed their bioenergetic functions and growth behaviors in vitro and in vivo. The mitochondrial oxygen consumption rates of cybrids were associated with quantitative parameters of components of metabolic syndrome such as body mass index, waist circumference, serum triglyceride levels and high-density lipoprotein cholesterol levels of donors. In addition, the cybrids showed different growth patterns both in vitro and in vivo, which were statistically different. Especially, the cybrids harboring mtDNA haplogroup D had a significantly slower growth rate. These findings suggest that mitochondrial genome could be a determinant of phenotypes of common complex diseases. Variations in mitochondrial genome as well as nuclear genome should be considered in explaining the genetic pathogenesis of common complex diseases.
• Bioblast editor: Kandolf G
Labels: MiParea: mtDNA;mt-genetics
Organism: Human
Affiliations
- Lee HK(1), Cho YM(2), Park KS(2), Pak YK(3), Tanaka M(4)
- Dept Int Med, Univ Eulji
- Seoul Nat Univ
- Dept Physiol, Kyung Hee Univ, Korea
- Dept Clin Lab, Tokyo Metro Geront Hosp, Japan. - [email protected]
References
- 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 80:407-15.
- Hwang S, Kwak SH, Bhak J, Kang HS, Lee YR, Koo BK, Park KS, Lee HK, Cho YM (2011) Gene expression pattern in transmitochondrial cytoplasmic hybrid cells harboring type 2 diabetes-associated mitochondrial DNA haplogroups. PLoS One 6:e22116.
- Wallace DC (2015) Mitochondrial DNA variation in human radiation and disease. Cell 163:33-8.
