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Obesity (Silver Spring). 2018 Aug;26(8):1303-1311. doi: 10.1002/oby.22206. Epub 2018 Jul 2.

The Vitamin K Epoxide Reductase Vkorc1l1 Promotes Preadipocyte Differentiation in Mice.

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State Key Laboratory of Genetic Engineering and National Center for International Research of Development and Disease, Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Key Laboratory of Magnetic Resonance in Biological Systems, State Key Laboratory of Magnetic Resonance and Atomic and Molecular Physics, National Centre for Magnetic Resonance, Wuhan Institute of Physics and Mathematics, University of Chinese Academy of Sciences, Wuhan, China.
State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Department of Genetics, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut, USA.
Department of Molecular, Cellular, and Developmental Biology, Howard Hughes Medical Institute, University of Colorado, Boulder, Colorado, USA.



Identification of novel regulators involved in adipose development is important to understand the molecular mechanism underlying obesity and associated metabolic disorders. Through isolation and analysis of a vitamin K epoxide reductase Vkorc1l1 mutant, this study aimed to disclose its function and underlying mechanism in adipose development and to obtain valuable insights regarding the mechanism of obesity.


A Vkorc1l1 mutation recovered from a forward genetic screen for obesity-related loci in mice was characterized to explore its effects in gene expression, animal metabolism, and adipose development. Adipogenesis was evaluated in both Vkorc1l1 mutant stromal vascular fraction and Vkorc1l1 knockdown preadipocytes. Intracellular vitamin K2 level and the effect of vitamin K2 on adipogenesis were tested in primary preadipocytes.


Vkorc1l1 mutants displayed a considerably lower fat to body weight ratio, substantially decreased plasma leptin, and significantly underdeveloped white adipose tissue. Adipogenic defects related with Vkorc1l1 deficiency were observed both in vivo and in vitro. Vitamin K2 could inhibit adipogenesis in stromal vascular fraction. Increased intracellular vitamin K2 level was detected in Vkorc1l1 mutant preadipocytes.


Vkorc1l1 promotes adipogenesis and possibly obesity. Downregulation of Vkorc1l1 increases intracellular vitamin K2 level and impedes preadipocyte differentiation.


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