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A pref-1-controlled non-inflammatory mechanism of insulin resistance

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机构： [1]College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada [2]Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China [3]College of Life and Environment Sciences, Wenzhou University, Wenzhou, Zhejiang, China [4]Institute of Cardiovascular Disease, Henan University of Chinese Medicine, Zhengzhou, Henan, China [5]Department of Cell and Molecular Physiology, Loyola University, Chicago, IL, USA [6]Department of Cardiology, The General Hospital of Chinese PLA, Beijing, China [7]Beijing Anding Hospital, Capital Medical University, Beijing, China [8]College of Life Sciences, Qingdao University, Qingdao, Shandong, China [9]Division of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John’s, NL, Canada [10]Guangdong Medical University, Zhanjiang, China [11]Division of Cardiac Rehabilitation, Department of Physical Medicine & Rehabilitation, Xiangya Hospital of Central South University, Changsha, Hunan, China [12]Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA [13]Department of Medical Biophysics, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada [14]Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA

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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.© 2023 The Authors.

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出版当年[2022]版：

大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

最新[2025]版：

大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

第一作者：

第一作者机构： [1]College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada

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通讯机构： [1]College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada [9]Division of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John’s, NL, Canada

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