Mitochondrial Dysfunction Markers in Paediatric Obesity:
DNA
Content and Oxidation Damage
Mailén Rojo, Andrea Liliana Millán, Alejandra Beatriz Duarte, Andrea Elena Iglesias Molli, Gustavo Daniel Frechtel, Gloria Edith Cerrone, Hernán Pérez ABSTRACT
Background
Childhood obesity increases chronic disease risk. Mitochondrial dysfunction, reflected by altered mitochondrial DNA (mtDNA) content and oxidative damage, has been implicated in obesity‐related metabolic disorders, but paediatric data remain scarce.
Objective
To evaluate mtDNA content and oxidation in children with obesity, stratified as metabolically healthy (MHO) or unhealthy (MUO), compared with peers with normal weight (NW).
Methods
Cross‐sectional study of 114 children aged 7–14 years: NW ( n = 37), MHO ( n = 40) and MUO ( n = 37). mtDNA content was measured by qPCR, and oxidative damage as 8‐oxoguanine by FPG‐qPCR. Analyses included Student's t ‐test, one‐way ANOVA with Tukey HSD, Pearson's χ 2 and linear regression adjusted for age, sex and Tanner stage.
Results
Children with obesity showed elevated cardiometabolic risk, lower HDL‐c, insulin resistance (IR), inflammation and significantly lower mtDNA content (−30.9%; p = 0.004) compared with NW, with no differences between MHO and MUO. Higher BMI was independently associated with lower mtDNA content (−3.72% per 1 kg/m 2 ; p = 0.003), consistent across pubertal stages. In a multivariable model of metabolic syndrome components, HDL‐c was independently associated with mtDNA content ( β = 0.33; p = 0.016). Lower mtDNA content was also associated with IR and higher hs‐CRP ( B = −0.13; p = 0.028). mtDNA oxidation showed only a non‐significant trend in obesity.
Conclusions
Lower mtDNA content was detectable in MHO and independently associated with HDL‐c and subclinical inflammation. The absence of MHO–MUO differences suggests that chronic inflammation and IR, common to both phenotypes, may be the main factors associated with mtDNA variation at this age.