Fig. 7.

Proposed model. After consuming a high-carbohydrate diet, activation of liver ER stress or the unfolded protein response (UPR) is required to induce lipid synthesis. SCD-1 is a target gene of Xbp-1s and increases MUFA synthesis to enable efficient TG and CE formation, subsequent VLDL formation, and eventual resolution of ER stress. However, in the absence of SCD-1, the inability to generate MUFA diminishes both TG and CE, with FC accumulating and further increasing ER stress/Xbp-1 splicing. FC conversion to oxysterols will lead to LXR activation, cholesterol efflux, and membrane remodeling in part through Cav-1 expression.