Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/100581
Title: Apelin attenuates oxidative stress in human adipocytes
Authors: Chen, Peng
Poh, Chueh Loo
Chong, Seow Khoon
Than, Aung
Zhang, Xiaohong
Leow, Melvin Khee-Shing
Keywords: DRNTU::Engineering::Bioengineering
Issue Date: 2014
Source: Than, A., Zhang, X., Leow, M. K.-S., Poh, C. L., Chong, S. K., & Chen, P. (2014). Apelin attenuates oxidative stress in human adipocytes. Journal of biological chemistry, 289(6), 3763-3774.
Series/Report no.: Journal of biological chemistry
Abstract: It has been recently recognized that the increased oxidative stress (ROS overproduction) in obese condition is a key contributor to the pathogenesis of obesity-associated metabolic diseases. Apelin is an adipocytokine secreted by adipocytes, and known for its anti-obesity and anti-diabetic properties. In obesity, both oxidative stress and plasma level of apelin are increased. However, the regulatory roles of apelin on oxidative stress in adipocytes remain unknown. In the present study, we provide evidence that apelin, through its interaction with apelin receptor (APJ), suppresses production and release of reactive oxygen species (ROS) in adipocytes. This is further supported by the observations that apelin promotes the expression of anti-oxidant enzymes via MAPK kinase/ERK and AMPK pathways, and suppresses the expression of pro-oxidant enzyme via AMPK pathway. We further demonstrate that apelin is able to relieve oxidative stress -induced dysregulations of the expression of anti- and pro- oxidant enzymes, mitochondrial biogenesis and function, as well as release of pro- and anti- inflammatory adipocytokines. This study, for the first time, reveals the antioxidant properties of apelin in adipocytes, and suggests its potential as a novel therapeutic target for metabolic diseases.
URI: https://hdl.handle.net/10356/100581
http://hdl.handle.net/10220/24131
DOI: http://dx.doi.org/10.1074/jbc.M113.526210
Rights: © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. This is the author created version of a work that has been peer reviewed and accepted for publication by Journal of Biological Chemistry, The American Society for Biochemistry and Molecular Biology, Inc. It incorporates referee’s comments but changes resulting from the publishing process, such as copyediting, structural formatting, may not be reflected in this document. The published version is available at: [http://dx.doi.org/10.1074/jbc.M113.526210].
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SCBE Journal Articles

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