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

Bing, Chen (2015) Is interleukin-1β a culprit in macrophage-adipocyte crosstalk in obesity? ADIPOCYTE, 4 (2). pp. 149-152.

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Abstract

Adipose tissue remodeling occurs in obesity, characterized by adipocyte hypertrophy and increased infiltration of macrophages which also shift to a proinflammatory phenotype. Factors derived from these macrophages significantly alter adipocyte function, such as repressing adipogenesis, inducing inflammatory response and desensitizing insulin action. As macrophages produce a cocktail of inflammatory signals, identifying the key factors that mediate the detrimental effects may offer effective therapeutic targets. IL-1β, a major cytokine produced largely by macrophages, is implicated in the development of obesity-associated insulin resistance. In this article, we discuss recent advances in our understanding of the role of IL-1β in macrophage-adipocyte crosstalk in obesity. IL-1β impairs insulin sensitivity in adipose tissue by inhibition of insulin signal transduction. Blocking the activity of IL-1β, its receptor binding or production improves insulin signaling and action in human adipocytes. This is in parallel with a reduction in macrophage-stimulated proinflammatory profile and lipolysis. Targeting IL-1β may be beneficial for protecting against obesity-related insulin resistance at the tissue and systemic levels.

Item Type:	Article
Uncontrolled Keywords:	interleukin-1 beta, obesity, adipose tissue, macrophage, adipocyte, inflammation, insulin resistance, cytokine, chemokine
Depositing User:	Symplectic Admin
Date Deposited:	23 Jun 2015 15:50
Last Modified:	14 Oct 2023 10:59
DOI:	10.4161/21623945.2014.979661
Related URLs:	Author Publisher
URI:	https://livrepository.liverpool.ac.uk/id/eprint/2014519