Mitochondrial DNA Copy Number in Peripheral Blood Is Independently Associated with Visceral Fat Accumulation in Healthy Young Adults

Aims. Visceral obesity is associated with an increased risk of cardiometabolic diseases and it is important to identify the underlying mechanisms. There is growing evidence that mitochondrial dysfunction is associated with metabolic disturbances related to visceral obesity. In addition, maintaining...

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Main Authors: Jee-Yon Lee, Duk-Chul Lee, Jee-Aee Im, Ji-Won Lee
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/2014/586017
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Summary:Aims. Visceral obesity is associated with an increased risk of cardiometabolic diseases and it is important to identify the underlying mechanisms. There is growing evidence that mitochondrial dysfunction is associated with metabolic disturbances related to visceral obesity. In addition, maintaining mitochondrial DNA (mtDNA) copy number is important for preserving mitochondrial function. Therefore, we investigated the relationship between mtDNA copy number and visceral fat in healthy young adults. Methods. A total of 94 healthy young subjects were studied. Biomarkers of metabolic risk factors were assessed along with body composition by computed tomography. mtDNA copy number was measured in peripheral leukocytes using real-time polymerase chain reaction (PCR) methods. Results. The mtDNA copy number correlated with BMI (r=-0.22, P=0.04), waist circumference (r=-0.23, P=0.03), visceral fat area (r=-0.28, P=-0.01), HDL-cholesterol levels (r=0.25, P=0.02), and hs-CRP (r=0.32, P=0.02) after adjusting for age and sex. Both stepwise and nonstepwise multiple regression analyses confirmed that visceral fat area was independently associated with mtDNA copy number (β=-0.33, P<0.01, β=0.32, and P=0.03, resp.). Conclusions. An independent association between mtDNA content and visceral adiposity was identified. These data suggest that mtDNA copy number is a potential predictive marker for metabolic disturbances. Further studies are required to understand the causality and clinical significance of our findings.
ISSN:1687-8337
1687-8345