The adipokine Retnla modulates cholesterol homeostasis in hyperlipidemic mice

Mi-Ran Lee, Chae-ji Lim, You-Han Lee, Jong-Gil Park, Seong Keun Sonn, Mi-Ni Lee, In-Hyuk Jung, Se-Jin Jeong, Sejin Jeon, Myoungsook Lee, Ki Sook Oh, Young Yang, Jae Bum Kim, Hueng-Sik Choi, Woojin Jeong, Tae-Sook Jeong, Won Kee Yoon, Hyoung Chin Kim, Jae-Hoon Choi and Goo Taeg Oh ()
Additional contact information
Mi-Ran Lee: Ewha Womans University
Chae-ji Lim: Ewha Womans University
You-Han Lee: Ewha Womans University
Jong-Gil Park: Ewha Womans University
Seong Keun Sonn: Ewha Womans University
Mi-Ni Lee: Ewha Womans University
In-Hyuk Jung: Ewha Womans University
Se-Jin Jeong: Ewha Womans University
Sejin Jeon: Ewha Womans University
Myoungsook Lee: Sungshin Women's University
Ki Sook Oh: Research Center for Women's Disease, Sookmyung Women's University
Young Yang: Research Center for Women's Disease, Sookmyung Women's University
Jae Bum Kim: National Creative Research Initiatives Center for Adipose Tissue Remodeling, Institute of Molecular Biology and Genetics, Seoul National University
Hueng-Sik Choi: National Creative Research Initiatives Center for Nuclear Receptor Signals, Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University
Woojin Jeong: Ewha Womans University
Tae-Sook Jeong: National Research Laboratory of Lipid Metabolism & Atherosclerosis, KRIBB
Won Kee Yoon: Biomedical Mouse Resource Center, KRIBB
Hyoung Chin Kim: Biomedical Mouse Resource Center, KRIBB
Jae-Hoon Choi: College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University
Goo Taeg Oh: Ewha Womans University

Nature Communications, 2014, vol. 5, issue 1, 1-15

Abstract: 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-α-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.

Date: 2014
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms5410 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5410

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms5410

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().