2026-06-14T03:53:27Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/271802026-01-27T01:16:01Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Fuentes, Lucía
author
Roszer, Tamás
author
Ricote, Mercedes
funder
Ministerio de Ciencia e Innovación (España)
funder
Fundación Genoma España
funder
Fundación La Marató TV3
funder
Marie Curie
2026-01-26T11:34:38Z
2026-01-26T11:34:38Z
2010
Mediators Inflamm. 2010:2010:219583.
Mediators of Inflammation
20508742
https://hdl.handle.net/20.500.12105/27180
Visceral 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.
eng
Inflammatory mediators and insulin resistance in obesity: role of nuclear receptor signaling in macrophages.
review
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URL
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File
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78b7fd1bd007c914ce8639159de8f99a
955457
application/pdf
Inflammatory mediators and insulin resistance_Mediators Inflamm_2010.pdf