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Received Jun 7, 2017; Accepted Aug 24, 2017
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1. Introduction
Obesity is associated with a state of mild inflammation, which can contribute to insulin resistance and type 2 diabetes mellitus [1]. This mild inflammatory condition is characterized by changes in the macrophage population in adipose tissue [2, 3]. An increase in proinflammatory type-1 macrophages (M1), which promotes insulin resistance, is evident in the adipose tissue of obese people, who also demonstrate reduced numbers of type-2 macrophages (M2), which are insulin sensitizing [4, 5].
Several studies have emphasized the role of interleukins (ILs) in the physiology of adipose cells: ILs increase lipolysis and modify body fat distribution and production of extracellular matrix by adipose tissue [6–8]. However, it was suggested that the interaction between adipose cells and the immune system is more complex than previously thought [9]. Some studies have shown that the activation of group 2 innate lymphoid cells (ILC2s) may modify the function of adipose tissue and systemic glucose homeostasis. It was observed that after IL-33 stimulation, eosinophils and ILC2s produce IL-4 and IL-13 [10–13], which are ILs that may promote the differentiation of adipose precursors into “brown like” adipocytes [14]. Additionally, IL-33 can influence the production of met-enkephalin by ILC2s, which can induce the process of “browning” in differentiated adipose cells [10]. Additionally, M2 macrophages that are activated by IL-4 can be mobilized in the subcutaneous adipose tissue, secreting catecholamines that activate brown adipocytes and induce the differentiation of beige adipocytes [14, 15]. We previously observed an elevation of thermogenic gene expression induced by cold that was increased by IL-4 in human adipocytes [16].
Despite the observed effect of IL-4 on the differentiation of beige adipocytes from precursor cells, the effects of IL-4 on differentiated adipocytes and its influence on the process of browning have yet to be investigated. Previous studies showed reduced IL-4 receptor (IL-4R) expression in differentiated...