Mitochondrial Dysfunction in Adipose Tissue and its Implication in the Onset of Type 2 Diabetes

Type 2 Diabetes has become one of the major causes of morbidity and mortality worldwide. This chronic metabolic disease, characterized by deficient production and secretion of insulin, has been increasing, and it is expected that the number will grow considerably in the coming years, causing massive health expenses. One of the actors associated with the pathogenesis of T2DM is the mitochondria; their dysfunction triggers insulin resistance due to cell failure and can occur at different sites. This study focuses primarily on adipose tissue, where excessive nutrient availability diminishes mitochondrial function and exacerbates reactive oxygen species (ROS) production, adipocyte apoptosis, local and systemic inflammation progression, thereby worsening insulin resistance and contributing to the onset of T2DM. The meta-analysis findings on mitochondrial membrane potential and PGC1-α expression in adipocytes underscore the profound influence of their changes in comparing healthy and obese individuals with comorbidities such as T2DM on the triggering of insulin resistance. Despite extensive research on T2DM, further investigation, particularly using quantitative methods to analyze mitochondrial biogenesis, is crucial. Such research is essential for developing targeted therapeutic interventions, with mitochondria being a primary focus of these efforts.