作者: Morihiro Matsuda , Hiroaki Yasumo , Mitsuyo Okazaki , Kazunori Fujimoto , Keita Kono
DOI: 10.1161/01.ATV.0000252827.51626.89
关键词:
摘要: Objectives— A low level of high-density lipoprotein (HDL) in plasma has been recognized as an aspect metabolic syndrome and a crucial risk factor cardiovascular events. However, the physiological regulation HDL levels not completely defined. Current studies aim to reveal contribution angiopoietin-like protein3 (angptl3), previously known suppressor lipase, metabolism. Methods Results— Angptl3-deficient mice showed cholesterol phospholipid (PL), which were increased by ANGPTL3 supplementation via adenovirus. In vitro, inhibited phospholipase activity endothelial lipase (EL), hydrolyzes HDL-PL hence decreases levels, through putative heparin-binding site N-terminal domain ANGPTL3. Post-heparin Angptl3-knockout had higher than did that wild-type mice, suggesting endogenous EL is elevated mice. Furthermore, we established ELISA system for human found significantly correlated with subjects. Conclusions— Angptl3 acts inhibitor may be involved humans rodents.