Study of the role of mitochondria dynamics in obesity-induced inflammation

Abstract

The growing interest in immunometabolism has been fueled by global Obesity epidemics and the recent findings indicate that Obesity affects the immune system and promotes inflammation. Inflammation induced by Obesity induces and aggravates a variety of chronic pathological conditions and diseases. The study of how the metabolism affects the immune response and how Obesity affects the systemic metabolism and modulates cellular immune function will provide new mechanisms to understand immunometabolic regulation in different pathological conditions. At the center of this regulation are mitochondria. These organelles are highly dynamic and undergo continuous elongation (fusion) and fragmentation (fission) processes, which results in the remodeling of cellular function. Obesity leads to low-grade systemic inflammation and subsequent insulin resistance. Adipose tissue resident macrophages play a central role in Obesity-induced inflammation. However, little is known about the role ofmitochondrial dynamics in the immunometabolic modulation of macrophages in the context of Obesity. Thus, our hypothesis is that inhibition of mitochondrial fission will result in lower activation of macrophages residing in adipose tissue, which would improve the inflammatory condition and insulin sensitivity. Thus, our aim is to determine how mitochondrial dynamics regulates the macrophage phenotype in both physiological and pathological conditions, such as Obesity. (AU)