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. 2017 Dec 19;8:117–131. doi: 10.1016/j.molmet.2017.12.008

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© 2017 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Proposed mechanisms by which PPARβ/δ regulates VLDLR levels and hepatic steatosis.Pparβ/δ deficiency may result in an increase in VLDLR levels and hepatic steatosis through several mechanisms. The activation of HRI caused by Pparβ/δ deficiency (reference [28]) and by activators of this kinase (BTdCPU) may increase the levels of VLDLR through the eIF2α-ATF4 pathway. ER stress can also activate the eIF2α-ATF4 pathway leading to an increase in the expression of VLDLR and FGF21. This hormone suppresses the eIF2α-ATF4 pathway through a negative feedback mechanism and thereby it also regulates the levels of VLDLR. ER stress also enhances the activity of Nrf2, a transcription factor reported to upregulate the expression of Fgf21 (reference [19]). Fructose feeding increases the levels of ROS and the activity of Nrf2 providing a mechanism for the increase of the levels of VLDLR. All these mechanisms may result in an increase in the levels of VLDLR causing hepatic steatosis. TG: triglyceride.