Abstract

Obesity is a growing global health concern, often linked to imbalances in how the body stores and uses energy. Our research focuses on understanding how fat cells regulate energy production and storage through their mitochondria, calls as the power plants of cell. In healthy conditions, these mitochondria adapt their shape and function depending on energy needs, helping the body respond to changes like fasting or overeating. However, in obesity, this adaptability is lost, and the mitochondria become fragmented, which reduces their ability to produce energy efficiently. We are investigating a small signaling protein called RalA, which appears to drive this mitochondrial fragmentation. Our early findings show that RalA becomes overactive in obesity, leading to changes in another protein activity, Drp1, which controls mitochondrial fission. By studying how RalA and Drp1 interact, we hope to uncover why mitochondrial function is impaired in obesity and how this contributes to metabolic disease. Ultimately, our goal is to identify new targets for therapies that can improve mitochondrial function in fat cells, potentially leading to better treatments for obesity and related conditions like diabetes and fatty liver disease.