Fuentes, LucíaRoszer, TamásRicote, Mercedes2026-01-262026-01-262010Mediators Inflamm. 2010:2010:219583.https://hdl.handle.net/20.500.12105/27180Visceral obesity is coupled to a general low-grade chronic inflammatory state characterized by macrophage activation and inflammatory cytokine production, leading to insulin resistance (IR). The balance between proinflammatory M1 and antiinflammatory M2 macrophage phenotypes within visceral adipose tissue appears to be crucially involved in the development of obesity-associated IR and consequent metabolic abnormalities. The ligand-dependent transcription factors peroxisome proliferator activated receptors (PPARs) have recently been implicated in the determination of the M1/M2 phenotype. Liver X receptors (LXRs), which form another subgroup of the nuclear receptor superfamily, are also important regulators of proinflammatory cytokine production in macrophages. Disregulation of macrophage-mediated inflammation by PPARs and LXRs therefore underlies the development of IR. This review summarizes the role of PPAR and LXR signaling in macrophages and current knowledge about the impact of these actions in the manifestation of IR and obesity comorbidities such as liver steatosis and diabetic osteopenia.Work performed in the authors’ laboratory was funded by awards to M. Ricote from the Spanish Ministry of Science and Innovation (SAF2009-07466), the “Ramon y ´ Cajal Programme,” the Fundacion “Genoma España,” and ˜ “Marato TV3,” to T. R ´ oszer from the “People” Marie ˝Curie Intra-European Fellowships Programme, Hungarian Research Fund (OTKA 76091), and “Mecenatura” Research Fund, and to L. Fuentes from the Spanish Ministry of Science and Innovation programme “Juan de la Cierva” and “People” Marie Curie European-Reintegration Fellowship programme. The CNIC is supported by the Spanish Ministry of Science and Innovation and by the Pro-CNIC Foundation. Simon Bartlett provided editorial assistance. The authors apologize to our many colleagues for not being able to cite all relevant references because of space limitations.engVoRhttp://creativecommons.org/licenses/by-nc-nd/4.0/Attribution-NonCommercial-NoDerivatives 4.0 International20508742Mediators of Inflammationopen access