u

can be mobilized during food deprivation. Under excess energy contribution to AT fibrosis remains elusive (Poggi et al., 2007; Saberi et al., 2009; Shi et al., 2006). Despite its importance in the dynamics of AT remodeling andconditions, AT expands through storage of fatty acids as triglyc-erides. AT expansion protects other organs against chronic lipid consequences on metabolic status, the mechanisms controlling AT fibrosis remain poorly understood. One of the limitations hasassociated with obesity and insulin resistance in hu-mans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte meta-bolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a func-tional Toll-like receptor 4 on adipose tissue hemato-poietic cells is necessary for the initiation of adipose tissue fibrosis. Continuous low-dose infusion of the Toll-like receptor 4 ligand, lipopolysaccharide, pro-motes adipose tissue fibrosis. Ex vivo, lipopolysac-charide-mediated induction of fibrosis is prevented by antibodies against the profibrotic factor TGFb1. Together, these results indicate that obesity and en-dotoxemia favor the development of adipose tissue fibrosis, a condition associated with insulin resis-tance, through immune cell Toll-like receptor 4