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. 2012 Aug 28;45(2):194–202. doi: 10.3109/07853890.2012.700116

Table II.

Effects of ER activation (this review, references (8,27,44)).

Up-regulation
 Synthesis—proteins, phospholipids, membranes
 IRE1α, ATF6α, PERK, XBP1, NF-kB
 Chaperones
 Apo AI gene, LDLR gene
 Cholesterol metabolism, oxysterol, and bile acid synthesis
 Receptors—LXRs, PPARs, PXR, CAR, LDLR
 Enzymes—P450s, LCAT, CCTα, glucokinase, FA desaturase
 Transporters—ABCA1, ABCG1, apo AI
 HDL-apo AI—anti-inflammatory, antioxidative, vasodilatative, antithrombotic activity
 Cholesterol efflux
Down-regulation/prevention
 Enzymes—HMGCoAR
 Apo B gene
Reparation
 Effects of inflammation and cellular stress, cell membranes
Change in risk factor
 Increase—HDL-C, HDL2-C, HDL-C/T-C, HDL2-C/HDL3-C, apo AI
 Decrease—LDL-C, cholesterol, triglycerides, LDL-C/HDL-C, apo B
Increase/normalization
 Glucose tolerance, metabolic clearance rate of glucose
 Insulin sensitivity, glucose disposal rate
Lowering/normalization/elimination
 Fasting blood glucose, insulin secretion, plasma IRI
 Insulin resistance, hyperinsulinemia
 Liver triglycerides, liver fat
 Amyloid β, Tau protein