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Nat Commun. 2014 Jul 15;5:4410. doi: 10.1038/ncomms5410.

The adipokine Retnla modulates cholesterol homeostasis in hyperlipidemic mice.

Author information

  • 1Department of Life Sciences, Ewha Womans University, Seoul 120-750, Republic of Korea.
  • 2Department of Food and Nutrition, Sungshin Women's University, #249-1, 3-ga, Dongsun-dong, Sungbuk-ku, Seoul 136-742, Republic of Korea.
  • 3Department of Life Science, Research Center for Women's Disease, Sookmyung Women's University, Seoul 140-742, Republic of Korea.
  • 4National Creative Research Initiatives Center for Adipose Tissue Remodeling, Department of Biological Sciences, Institute of Molecular Biology and Genetics, Seoul National University, Seoul 151-742, Republic of Korea.
  • 5National Creative Research Initiatives Center for Nuclear Receptor Signals, Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju 500-751, Republic of Korea.
  • 6National Research Laboratory of Lipid Metabolism & Atherosclerosis, KRIBB, Daejeon 305-806, Republic of Korea.
  • 7Biomedical Mouse Resource Center, KRIBB, Chungbuk 363-883, Republic of Korea.
  • 8Department of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul, 133-791, Republic of Korea.


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.

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