Open AccessCREBH regulation of lipid metabolism through multifaceted functions that improve arteriosclerosis
Author(s) -
Nakagawa Yoshimi,
Matsuzaka Takashi,
Shimano Hitoshi
Publication year - 2022
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/jdi.13766
Subject(s) - chylomicron , medicine , endocrinology , very low density lipoprotein , apolipoprotein b , lipoprotein , lipoprotein lipase , ldl receptor , triglyceride , lrp1 , apolipoprotein e , receptor , cholesterol , chemistry , disease , adipose tissue
Cyclic adenosine monophosphate‐responsive element‐binding protein H (CREBH) activates lipoprotein lipase (LPL) activity by modulating apolipoproteins. Activated LPL hydrolyzes triglyceride‐rich lipoproteins, such as very low‐density lipoprotein (VLDL) and chylomicrons, resulting in remnant lipoproteins. CREBH increases apolipoprotein E (ApoE), a ligand that mediates the clearance of remnant particles and reduces ApoC3, which interferes with remnant clearance. CREBH also improves VLDL receptor (VLDLR) and LDL receptor‐related protein 1 (LRP1) protein that mediates remnant clearance. Therefore, CREBH promotes the clearance of remnant particles from the blood, decreasing the atherogenic plaque area. CREBH induces the secretion of fibroblast growth factor 21 (FGF21) into the blood, decreasing plasma triglyceride. CREBH produces ApoA1 and so increases plasma HDL‐cholesterol levels.