PID1 in adipocytes modulates whole-body glucose homeostasis |
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Authors: | Ling Chen Xing-Yun Wang Jin-Gai Zhu Liang-Hui You Xing Wang Xian-Wei Cui Chun-Mei Shi Fang-Yan Huang Ya-Hui Zhou Lei Yang Ling-Xia Pang Yao Gao Chen-Bo Ji Xi-Rong Guo |
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Affiliation: | Nanjing Maternal and Child Health Hospital, Nanjing 210004, China;Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing 210004, China |
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Abstract: | The novel obesity-associated protein Phosphotyrosine Interaction Domain containing 1 (PID1) inhibits insulin-PI3K/Akt signaling pathway and insulin-stimulated glucose uptake in vitro. In this study, we generated fat tissue-specific aP2-PID1 transgenic (aP2-PID1tg) mice and PID1 knockout (PID1?/?) mice to explore how PID1 affects glucose metabolism in vivo. We observed insulin resistance and impaired insulin-PI3K/Akt signaling in aP2-PID1tg mice. Consistent with these data, the PID1?/? mice displayed improved glucose tolerance and insulin sensitivity under chow diet, with increased Akt phosphorylation in white adipose tissue (WAT). We further demonstrated that PID1 could interact with low density lipoprotein receptor-related protein 1 (LRP1) but not the insulin receptor (IR) in adipocytes, and its overexpression could lead to decreased GLUT4 level. Our results thus indentify PID1 as a critical regulator of glucose metabolism in adipocytes. |
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Keywords: | PID1 Insulin resistance LRP1 GLUT4 |
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