| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8300404 | Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms | 2018 | 8 Pages |
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 (PID1â/â) 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 PID1â/â 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.
Keywords
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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,