This lecture delves into the pivotal role of adipose tissue in obesity and its response to weight loss, particularly via bariatric surgery. Adipose tissue, responsible for storing excess energy, undergoes significant changes during obesity, marked by inflammation and fibrosis. Bariatric surgery, serving as a model, allow the exploration of adipose tissue remodeling post-weight loss, inducing metabolic and fibro-inflammatory shifts. Despite successful weight loss, inflammation and fibrosis persist, as evidenced by changes in immune cells, altered cytokine profiles and the accumulation of extracellular matrix (ECM). Unfortunately, these lingering effects impair the normal adipose tissue function. In this context, adipose progenitors, an heterogenous resident population of mesenchymal stromal cells, display functions important to fibrosis development, capable of differentiating into myofibroblasts and contributing to ECM deposition. Particularly, a distinct subpopulation of adipose progenitors with high CD9 expression (CD9high) is associated with fibrosis and insulin resistance in human obesity. The persistence of fibrosis post-weight loss poses challenges, correlating with metabolic dysfunction despite improved glucose tolerance. A comprehensive understanding of the mechanisms driving adipose tissue remodeling and fibrosis post-weight loss is imperative for the development of effective treatments for obesity. The intricate interplay between adipose tissue, inflammation, and fibrosis underscores the necessity for further in-depth research to elucidate these mechanisms and formulate targeted therapies for obesity-related complications.