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Childhood (pediatric) obesity is becoming increasingly common at an alarming rate. Obese children are more likely to develop insulin resistance, relative insulin insufficiency, and type 2 diabetes. Recent research suggests that mitochondrial dysfunction is related to, and may be predictive of, insulin resistance among adult relatives of type 2 diabetes patients. Mitochondria produce ATP, which is used to create energy, especially in muscle tissue, and they play a role in glucose and fat metabolism. Mitochondrial dysfunction plays a role in the development of metabolic diseases. Affected tissues include adipose, liver, and skeletal muscle, which all contribute to food metabolism. Since cells require a balance between mitochondrial ATP generation through oxidative phosphorylation (OXPHOS) and proton gradient dissipation to avoid damage caused by reactive oxygen species (ROS), abnormal mitochondrial function leads to fat buildup and insulin resistance. Obesity, insulin resistance, and type 2 diabetes (T2D) are all caused by growth and transcription factors that influence mitochondrial gene expression. On the other hand, obesity and hypertension both impair heart mitochondrial biogenesis and function. By promoting the expression of chaperones, SIRT1, and antioxidants, moderate weight reduction reduces systemic inflammation and improves mitochondrial dysfunction. In this review, the variables that relate mitochondrial dysfunction to pediatric obesity are discussed.