Is interleukin-1b a culprit in macrophage-adipocyte crosstalk in obesity?

Adipose tissue remodeling occurs inobesity, characterized by adipocyte hypertrophy and increased infiltration of macrophages which also shift to a proin-flammatory phenotype. Factors derived from these macrophages significantly alter adipocyte function, such as repres-sing adipogenesis, inducing inflamma-tory response and desensitizing insulin action. As macrophages produce a cock-tail of inflammatory signals, identifying the key factors that mediate the detri-mental effects may offer effective thera-peutic targets. IL-1b, a major cytokine produced largely by macrophages, is implicated in the development of obe-sity-associated insulin resistance. In this article, we discuss recent advances in our understanding of the role of IL-1b in macrophage-adipocyte crosstalk in obe-sity. IL-1b impairs insulin sensitivity in adipose tissue by inhibition of insulin signal transduction. Blocking the activity of IL-1b, its receptor binding or produc-tion improves insulin signaling and action in human adipocytes. This is in parallel with a reduction in macrophage-stimulated proinflammatory profile and lipolysis. Targeting IL-1b may be benefi-cial for protecting against obesity-related insulin resistance at the tissue and sys-temic levels