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

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). 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. 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). A lower mtDNA copy number and higher deletion ratio were independent predictors for new-onset MetS in a general population exposed to the pesticide.