Obesity can be defined as the adaptive response of organism facing chronic nutrient overflow. In this context, the adipose tissue (AT) can expand, through increased adipocyte size and number, to function as the main energy-storing organ. However, over the course of obesity progression, the AT undergo continual remodeling, evolving into pathological alterations. It is now clear that pro-inflammatory cell accumulation favors local AT injury. More recently, we and others described excess levels of extracellular matrix (ECM) and fibrosis in AT depots from obese individuals. In obese mice, targeting ECM-remodeling improves glucose tolerance and insulin sensitivity. Therefore AT fibrosis represents a maladaptive mechanism contributing to obesity-related metabolic complications such as diabetes, cardiometabolic and liver diseases. Here, we review the current knowledge about obesity-induced adipose tissue remodeling and its local and systemic consequences.
© 2018 médecine/sciences – Inserm.