ABSTRACT
Obesity has reached astounding levels worldwide that tackling this disease has been an ongoing effort of the medical and research community. However, there are still lacking therapies that can promote both sustained weight loss and metabolic improvement. Understanding the pathophysiology of obesity might take us a step closer to reach this type of therapeutic approaches. The cellular hallmarks of obesity such as inflammation and endoplasmatic reticulum stress, can promote mitochondrial dysfunction in the central nervous system and in peripheral organs. The impairment of the mitochondria within the cell, and therefore the compromise of the cellular power plant, will eventually promote cell death. Mitochondria dysfunction will compromise the regulation of energetic balance within the hypothalamus, the key regulator of metabolic homeostasis, as well as the response of peripheral organs such as white adipose tissue. Thus, mitochondria dysfunction in obesity is on one hand a hallmark of the pathophysiology of obesity and on the other, a trigger per se of obese phenotype. Elucidating the mechanisms of mitochondrial dysfunction in obesity, both at central nervous system and periphery will pave the way to better therapeutic approaches.
