ArticleAntioxidants (Basel, Switzerland)2019
PON2 Deficiency Leads to Increased Susceptibility to Diet-Induced Obesity.
Article in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Adipose Tissue-Central Nervous System Axis in Obesity: Molecular Mechanisms, Inflammation, and Nutritional and Technological Implications.Metabolites · 2026Review
- Paraoxonase 2 as a target for aging-related diseases.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Review
- Insights into the molecular and genetic role of obesity in breast cancer pathogenesis.Cancer biology & therapy · 2025Review
- The Paraoxonase (International journal of molecular sciences · 2025Review
- Neurotherapeutic effects of Vutiglabridin as a Paraoxonase-2 modulator in preclinical models of Parkinson's disease.Molecular neurodegeneration · 2025Article
- Effect ofBiomolecules · 2025Article
- A Case-Control Study Supports Genetic Contribution of theAntioxidants (Basel, Switzerland) · 2024Article
- Differential expression of cardiometabolic and inflammation markers and signaling pathways between overweight/obese Qatari adults with high and low plasma salivary α-amylase activity.Frontiers in endocrinology · 2024Article
- Paraoxonase 2 Deficiency Causes Mitochondrial Dysfunction in Retinal Pigment Epithelial Cells and Retinal Degeneration in Mice.Antioxidants (Basel, Switzerland) · 2023Article
- Vutiglabridin Modulates Paraoxonase 1 and Ameliorates Diet-Induced Obesity in Hyperlipidemic Mice.Biomolecules · 2023Article
- Effect of Mechanical Stimuli and Zoledronic Acid on the Femoral Bone Morphology in Rats with Obesity and Limited Mobility.Journal of clinical medicine · 2022Article
- Structural variants and tandem repeats in the founder individuals of four FBMC genomics · 2022Article
- Examining the role of paraoxonase 2 in the dopaminergic system of the mouse brain.BMC neuroscience · 2022Article
- CircHIPK3 prevents chondrocyte apoptosis and cartilage degradation by sponging miR-30a-3p and promoting PON2.Cell proliferation · 2022Article
- Mitochondrial regulation and white adipose tissue homeostasis.Trends in cell biology · 2022Review
- Coronary Heart Disease in Type 2 Diabetes Mellitus: Genetic Factors and Their Mechanisms, Gene-Gene, and Gene-Environment Interactions in the Asian Populations.International journal of environmental research and public health · 2022Review
- Insights into the role of paraoxonase 2 in human pathophysiology.Journal of biosciences · 2022Article
- The Structure and Function of Paraoxonase-1 and Its Comparison to Paraoxonase-2 and -3.Molecules (Basel, Switzerland) · 2020Review
- Association of Genetic and Environmental Factors with Non-Alcoholic Fatty Liver Disease in a Chinese Han Population.International journal of environmental research and public health · 2020Article
- Paraoxonases Activities and Polymorphisms in Elderly and Old-Age Diseases: An Overview.Antioxidants (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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.
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