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COMMENTARIES

Erythropoietin and obesity-induced white adipose tissue inflammation: redefining the boundaries of the immunometabolism territory

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Pages 153-157 | Received 07 Jul 2014, Accepted 15 Oct 2014, Published online: 07 Jan 2015
 

Abstract

The adipose tissue represents a critical and predominant site for the interaction between metabolic and inflammatory responses during health and disease. In the white adipose tissue microenvironment, macrophages/adipocytes cross-talk have been shown to influence the metabolic and inflammatory states of both cell types, and contribute to the development of systemic insulin resistance during obesity. Indeed, the existence of paracrine loops between mature adipocytes and macrophages, especially during obesity-induced stress, involving the release of, and response to, an array of cytokines and regulatory factors, have been extensively studied using several in vitro and in vivo model systems. Published evidence together with recent observations, brought to light the unexpected role of erythropoietin and its receptor in the regulation of white adipose tissue mass, energy homeostasis, and inflammation as demonstrated by erythropoietin effects on adipocyte development and metabolic profile, and macrophage infiltration, cytokine responses, and activation state during diet-induced obesity. In this commentary, we discuss the newly added elements and perspectives to our understanding of the erythropoietin/erythropoietin-receptor axis as a regulator of obesity-induced white adipose tissue inflammation, providing insight into its effects on cytokine responses of macrophages and adipocytes, and possible links to glucose metabolism and insulin resistance.

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Acknowledgments

This work was supported by the Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health (ZIA/DK025102).

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