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Obesity, DNA Damage, and Development of Obesity-Related Diseases

Department of Biochemistry and Pharmacogenomics, Faculty of Pharmacy with Division of Laboratory Medicine, Medical University of Warsaw, Banacha 1B, 02-097 Warsaw, Poland
Centre for Preclinical Research, Medical University of Warsaw, Banacha 1B, 02-097 Warsaw, Poland
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(5), 1146;
Received: 25 January 2019 / Revised: 28 February 2019 / Accepted: 2 March 2019 / Published: 6 March 2019
(This article belongs to the Special Issue Molecular Research on Metabolic Disorders)
PDF [1427 KB, uploaded 6 March 2019]


Obesity has been recognized to increase the risk of such diseases as cardiovascular diseases, diabetes, and cancer. It indicates that obesity can impact genome stability. Oxidative stress and inflammation, commonly occurring in obesity, can induce DNA damage and inhibit DNA repair mechanisms. Accumulation of DNA damage can lead to an enhanced mutation rate and can alter gene expression resulting in disturbances in cell metabolism. Obesity-associated DNA damage can promote cancer growth by favoring cancer cell proliferation and migration, and resistance to apoptosis. Estimation of the DNA damage and/or disturbances in DNA repair could be potentially useful in the risk assessment and prevention of obesity-associated metabolic disorders as well as cancers. DNA damage in people with obesity appears to be reversible and both weight loss and improvement of dietary habits and diet composition can affect genome stability. View Full-Text
Keywords: DNA damage; obesity; inflammation; oxidative stress; ROS; cancer DNA damage; obesity; inflammation; oxidative stress; ROS; cancer

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Włodarczyk, M.; Nowicka, G. Obesity, DNA Damage, and Development of Obesity-Related Diseases. Int. J. Mol. Sci. 2019, 20, 1146.

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