The Association between Obesity and Mitochondrial Dysfunction: A Mini Review

Abstract

In times where the prevalence of obesity increases steadily and has become one of the so called “top killers” of the world, it is necessary to understand more how obesity affects our body and more importantly why it affects our body in that manner. To do that this article will emphasize on the bidirectional relationship between obesity and mitochondrial dysfunction.  Overall said it appears that in patients suffering from obesity the total number of mitochondria seems to decrease in the different tissues due to an increase in production of the Tumor necrosis factor alpha (TNFa), which stimulates the extrinsic apoptotic pathway. However, it is of high importance to notice that the effects of obesity differ from tissue to tissue (as discussed later). Likewise, the production of Reactive Oxygen Species (ROS) inside the mitochondria, seems to increase also. This increase in ROS is often also associated with damage of the mitochondrial DNA (mtDNA) leading to mutations that may affect important metabolic pathways in the human body. Following mutations in the mitochondrial DNA can also be inherited in a maternal fashion and can lead to metabolic disorders like diabetes.  Moreover, it is important to mention that the effects of obesity will also differ from woman to men, because of hormonal reasons that cause different fat deposits in men (more visceral fat) compared to women, that tend to have higher fat deposits at gluteal and femoral subcutaneous regions. On the other hand, there is also a lot of evidence that supports the thesis of mitochondrial dysfunction leading to obesity. For example, in elderly people the volume of mtDNA decreases and may result also in metabolic changes. To conclude, this article gives some possible ideas on how mitochondrial dysfunction could be treated