iScience · 2023
A pref-1-controlled non-inflammatory mechanism of insulin resistance.
СтатьяНазвание и аннотация: Перевод в очереди
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Huang Yiheng, Cui Donghong, Chen Liujun, Tong Haibin, Wu Hong, Muller Grace K, Qi Yadan, Wang Shuxia, Xu Jinjie, Gao Xiang, Fifield Kathleen E, Wang Lingyan, Xia Zhengyuan, Vanderluit Jacqueline L, Liu Suixin, Leng Lin, Sun Guang, McGuire John, Young Lawrence H, Bucala Richard, Qi Dake
Аннотация
While insulin resistance (IR) is associated with inflammation in white adipose tissue, we report a non-inflammatory adipose mechanism of high fat-induced IR mediated by loss of Pref-1. Pref-1, released from adipose Pref-1+ cells with characteristics of M2 macrophages, endothelial cells or progenitors, inhibits MIF release from both Pref-1+ cells and adipocytes by binding with integrin β1 and inhibiting the mobilization of p115. High palmitic acid induces PAR2 expression in Pref-1+ cells, downregulating Pref-1 expression and release in an AMPK-dependent manner. The loss of Pref-1 increases adipose MIF secretion contributing to non-inflammatory IR in obesity. Treatment with Pref-1 blunts the increase in circulating plasma MIF levels and subsequent IR induced by a high palmitic acid diet. Thus, high levels of fatty acids suppress Pref-1 expression and secretion, through increased activation of PAR2, resulting in an increase in MIF secretion and a non-inflammatory adipose mechanism of IR.