The adipokine Retnla modulates cholesterol homeostasis in hyperlipidemic mice
- Authors
- Lee, Mi-Ran; Lim, Chae-ji; Lee, You-Han; Park, Jong-Gil; Sonn, Seong Keun; Lee, Mi-Ni; Jung, In-Hyuk; Jeong, Se-Jin; Jeon, Sejin; Lee, Myoungsook; Oh, Ki Sook; Yang, Young; Kim, Jae Bum; Choi, Hueng-Sik; Jeong, Woojin; Jeong, Tae-Sook; Yoon, Won Kee; Kim, Hyoung Chin; Choi, Jae-Hoon; Oh, Goo Taeg
- Issue Date
- Jul-2014
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- NATURE COMMUNICATIONS, v.5
- Journal Title
- NATURE COMMUNICATIONS
- Volume
- 5
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10858
- DOI
- 10.1038/ncomms5410
- ISSN
- 2041-1723
- Abstract
- Hyperlipidemia is a well-recognized risk factor for atherosclerosis and can be regulated by adipokines. Expression of the adipokine resistin-like molecule alpha (Retnla) is regulated by food intake; whether Retnla has a role in the pathogenesis of hyperlipidemia and atherosclerosis is unknown. Here we report that Retnla has a cholesterol-lowering effect and protects against atherosclerosis in low-density lipoprotein receptor-deficient mice. On a high-fat diet, Retnla deficiency promotes hypercholesterolaemia and atherosclerosis, whereas Retnla overexpression reverses these effects and improves the serum lipoprotein profile, with decreased cholesterol in the very low-density lipoprotein fraction concomitant with reduced serum apolipoprotein B levels. We show that Retnla upregulates cholesterol-7-alpha-hydroxylase, a key hepatic enzyme in the cholesterol catabolic pathway, through induction of its transcriptional activator liver receptor homologue-1, leading to increased excretion of cholesterol in the form of bile acids. These findings define Retnla as a novel therapeutic target for treating hypercholesterolaemia and atherosclerosis.
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