Journal
BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
Volume 1861, Issue 2, Pages 125-132Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbagrm.2018.01.001
Keywords
PIDI; Insulin resistance; LRP1; GLUT4
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Funding
- National Key Basic Research Program of China [2013CB530604]
- National Natural Science Foundation of China [81270928]
- Science & Technology Development Foundation of Nanjing Medical University [2015NJMUZD057]
- Graduate Student Research Innovation Project of Jiangsu Province [CXZZ13-05]
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The novel obesity-associated protein Phosphotyrosine Interaction Domain containing 1 (PIDI) 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-PIDtg) 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-PID1(tg) 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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