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Antioxidants 2019, 8(1), 19; https://doi.org/10.3390/antiox8010019

PON2 Deficiency Leads to Increased Susceptibility to Diet-Induced Obesity

1
Division of Cardiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
2
Department of Human Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA
3
Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA 90095, USA
4
Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
5
Department of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
6
Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA
7
Department of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095, USA
*
Author to whom correspondence should be addressed.
Received: 5 December 2018 / Revised: 5 January 2019 / Accepted: 8 January 2019 / Published: 11 January 2019
(This article belongs to the Special Issue Paraoxonases in Oxidation and Inflammation)
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Abstract

(1) Background: Paraoxonase 2 (PON2) is a ubiquitously expressed protein localized to endoplasmic reticulum and mitochondria. Previous studies have shown that PON2 exhibits anti-oxidant and anti-inflammatory functions, and PON2-deficient (PON2-def) mice are more susceptible to atherosclerosis. Furthermore, PON2 deficiency leads to impaired mitochondrial function. (2) Methods: In this study, we examined the susceptibility of PON2-def mice to diet-induced obesity. (3) Results: After feeding of an obesifying diet, the PON2-def mice exhibited significantly increased body weight due to increased fat mass weight as compared to the wild-type (WT) mice. The increased adiposity was due, in part, to increased adipocyte hypertrophy. PON2-def mice had increased fasting insulin levels and impaired glucose tolerance after diet-induced obesity. PON2-def mice had decreased oxygen consumption and energy expenditure. Furthermore, the oxygen consumption rate of subcutaneous fat pads from PON2-def mice was lower compared to WT mice. Gene expression analysis of the subcutaneous fat pads revealed decreased expression levels of markers for beige adipocytes in PON2-def mice. (4) Conclusions: We concluded that altered systemic energy balance, perhaps due to decreased beige adipocytes and mitochondrial dysfunction in white adipose tissue of PON2-def mice, leads to increased obesity in these mice. View Full-Text
Keywords: obesity; mitochondrial function; antioxidant obesity; mitochondrial function; antioxidant
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Shih, D.M.; Meng, Y.; Sallam, T.; Vergnes, L.; Shu, M.L.; Reue, K.; Tontonoz, P.; Fogelman, A.M.; Lusis, A.J.; Reddy, S.T. PON2 Deficiency Leads to Increased Susceptibility to Diet-Induced Obesity. Antioxidants 2019, 8, 19.

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