Treatment with EC induced mitochondrial biogenesis and positive changes in mitochondrial dynamics (fission and fusion) and activity, as measured indirectly by changes in citrate synthase and <i>Ucp3</i> expression.<h4>Discussion</h4>Results reinforce the potential of EC as a modulator of mitochondrial function in dysfunctional conditions associated with obesity, thereby attenuating the mechanisms underlying sarcopenia. The gene discussed is UCP3; the disease is obesity due to melanocortin 4 receptor deficiency.