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. 2020 Jun 9;11:365. doi: 10.3389/fendo.2020.00365

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Copyright © 2020 Ge, Yang, Zhou, Wang, Li and Tong.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The role of the PPP in insulin resistance. (A) CARKL is highly expressed in M2 macrophages, limiting the PPP flux by inhibiting G6PD. M2 macrophages release anti-inflammatory mediators including IL-10 and arginase 1 to maintain insulin sensitivity. Decreased G6PD in adipocytes suppresses inflammation and ameliorates insulin resistance. (B) FFAs and pro-inflammatory cytokines including TNF-α, IL-1β, and resistin increase G6PD expression in both adipocytes and M1 macrophages, which stimulate inflammatory responses leading to insulin resistance.