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ObjectiveThe objective of this study was to examine associations between umbilical cord mitochondrial DNA copy number (mtDNAcn) and adiposity across childhood.MethodsIn a prospective birth cohort of Dominican and African American children from New York City, New York (1998–2006), mtDNAcn was measured in cord blood. Children (N = 336) were evaluated for their height, weight, and bioimpedance at age 5, 7, 9, and 11 years. We used linear mixed‐effects models to assess associations of mtDNAcn tertiles in cord blood with child BMI, BMI z scores, fat mass index, and body fat percentage. Latent class growth models and interactions between mtDNAcn and child age or child age2 were used to assess associations between age and adiposity trajectories.ResultsBMI was, on average, 1.5 kg/m2 higher (95% CI: 0.58, 2.5) in individuals with mtDNAcn in the low‐ compared with the middle‐mtDNAcn tertile. Results were similar for BMI z score, fat mass index, and body fat percentage. Moreover, children in the low‐mtDNAcn group had increased odds of being in an “increasing” or “high‐stable” adiposity class.ConclusionsLower mtDNAcn at birth may predict greater childhood adiposity, highlighting the potential key role of perinatal mitochondrial function in adiposity during development.
ObjectiveThe objective of this study was to examine associations between umbilical cord mitochondrial DNA copy number (mtDNAcn) and adiposity across childhood.MethodsIn a prospective birth cohort of Dominican and African American children from New York City, New York (1998–2006), mtDNAcn was measured in cord blood. Children (N = 336) were evaluated for their height, weight, and bioimpedance at age 5, 7, 9, and 11 years. We used linear mixed‐effects models to assess associations of mtDNAcn tertiles in cord blood with child BMI, BMI z scores, fat mass index, and body fat percentage. Latent class growth models and interactions between mtDNAcn and child age or child age2 were used to assess associations between age and adiposity trajectories.ResultsBMI was, on average, 1.5 kg/m2 higher (95% CI: 0.58, 2.5) in individuals with mtDNAcn in the low‐ compared with the middle‐mtDNAcn tertile. Results were similar for BMI z score, fat mass index, and body fat percentage. Moreover, children in the low‐mtDNAcn group had increased odds of being in an “increasing” or “high‐stable” adiposity class.ConclusionsLower mtDNAcn at birth may predict greater childhood adiposity, highlighting the potential key role of perinatal mitochondrial function in adiposity during development.
Mitochondria are essential organelles within cells, playing various roles in numerous cellular processes, including differentiation, growth, apoptosis, energy conversion, metabolism, and cellular immunity. The phenotypic variation of mitochondria is specific to different tissues and cell types, resulting in significant differences in their function, morphology, and molecular characteristics. Asthma is a chronic, complex, and heterogeneous airway disease influenced by external factors such as environmental pollutants and allergen exposure, as well as internal factors at the tissue, cellular, and genetic levels, including lung and airway structural cells, immune cells, granulocytes, and mast cells. Therefore, a comprehensive understanding of the specific responses of mitochondria to various external environmental stimuli and internal changes are crucial for elucidating the pathogenesis of asthma. Previous research on mitochondrial-targeted therapy for asthma has primarily focused on antioxidants. Consequently, it is necessary to summarize the multifaceted roles of mitochondria in the pathogenesis of asthma to discover additional strategies targeting mitochondria in this context. In this review, our goal is to describe the changes in mitochondrial function in response to various exposure factors across different cell types and other relevant factors in the context of asthma, utilizing a new mitochondrial terminology framework that encompasses cell-dependent mitochondrial characteristics, molecular features, mitochondrial activity, function, and behavior.
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