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. 2015 Oct 20;5(10):e661. doi: 10.1038/tp.2015.161

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Copyright © 2015 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Schematic diagrams illustrating the mechanism of (a) the involvement of PGRMC1/INSIG/SCAP/SREBP signaling in the lipid biosynthesis. (b) AAPD-induced hepatic inhibition of PGRMC1/INSIG-2 and subsequent activation of SCAP/SREBP that contributes to the increased biosynthesis of lipids in the liver. The add-on MIF treatment can reverse AAPD-induced metabolic disturbances by upregulating the expression of PGRMC1/INSIG-2 followed by downregulation of SCAP/SREBP. AAPD, atypical antipsychotic drug; aSREBP, active sterol-regulatory element-binding protein; ER, endoplasmic reticulum; FA, fatty acid; iaSREBP, inactive sterol-regulatory element-binding protein; INSIG, insulin-induced gene; MIF, mifepristone; PGRMC1, progesterone receptor membrane component 1; SCAP, SREBP-cleavage activating protein; TAG, triacylglycerol.