Mitochondrial DNA content and deletion ratio are associated with metabolic syndrome in a general population exposed to pesticide

Jung Ran Choi, Sungjin Park, Sung Kyung Kim, Jae Yeop Kim, Kyungsuk Lee, Sung Soo Oh, Sang Baek Koh

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Abstract

Background: Mitochondrial DNA (mtDNA) copy number and deletion ratio may be asymmetrically determined using physiologic or pathologic conditions. Mitochondrial dysfunction is associated with an increased risk of developing metabolic syndrome (MetS). Objective: Here, we investigated the association between mtDNA copy number and/or deletion ratio and the risk of developing MetS in a general population exposed to the pesticide. We examined 215 randomly sampled adults who were exposed to pesticide but did not present with MetS in a prospective cohort study. Both mtDNA copy number and deletion ratio were determined using quantitative real-time polymerase chain reaction. Results: During the average 2.8-year follow-up period, 76 (35.3%) participants developed new-onset MetS. The numbers of mtDNA copies were significantly lower in participants with new-onset MetS than in those without MetS (112.15 ± 26.15 vs. 133.13 ± 44.44, p < 0.001), whereas the mtDNA deletion ratios were higher in participants with MetS than in those without MetS (10.59 ± 11.96 vs. 4.52 ± 6.74, p < 0.001). In the multivariate-adjusted models, the participants with a higher tertile of mtDNA copy number were 0.355 times more likely to develop MetS than those with the lowest tertile [odds ratio (OR) 0.355, 95% confidence interval (CI) 0.150–0.841, p = 0.004]. A higher mtDNA deletion ratio was significantly associated with the risk of developing MetS in populations exposed to pesticide (OR 5.062, 95% CI 1.164–22.004, p = 0.004). Conclusion: A lower mtDNA copy number and higher deletion ratio were independent predictors for new-onset MetS in a general population exposed to the pesticide.

Original languageEnglish
Pages (from-to)347-354
Number of pages8
JournalMolecular and Cellular Toxicology
Volume16
Issue number3
DOIs
Publication statusPublished - 2020 Jul 1

Bibliographical note

Funding Information:
This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education (2017R1D1A3B03034119). Moreover, this research was supported by the Medical Research Center Program 2017R1A5A2015369. This work was carried out with the support of the Cooperative Research Program for Agriculture Science & Technology Development (project no.: PJ01250901) Rural Development Administration, Republic of Korea. This work was supported (in part) by the Yonsei University Research Fund of 2017.

Publisher Copyright:
© 2020, The Korean Society of Toxicogenomics and Toxicoproteomics 2020.

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Toxicology
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

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