Peroxiredoxin 5 ameliorates obesity-induced non-alcoholic fatty liver disease through the regulation of oxidative stress and AMP-activated protein kinase signaling

Kim, Mi Hye; Seong, Jung Bae; Huh, Jae‐Won; Bae, Yong Chul; Lee, Hyun‐Shik; Lee, Dong‐Seok

doi:10.1016/j.redox.2019.101315

Cited by 60 publications

(55 citation statements)

References 50 publications

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“…Future studies using these new models, as well as complete knockout mouse models, will help us better understand the physiological roles of PRDXs and provide possible therapeutic targets for drugs against diseases, such as cancer and inflammatory and metabolic diseases. [94,96] High-fat diet Fat, liver…”

Section: Discussionmentioning

confidence: 99%

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Knockout Mouse Models for Peroxiredoxins

Lee

2020

Antioxidants

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Peroxiredoxins (PRDXs) are members of a highly conserved peroxidase family and maintain intracellular reactive oxygen species (ROS) homeostasis. The family members are expressed in most organisms and involved in various biological processes, such as cellular protection against ROS, inflammation, carcinogenesis, atherosclerosis, heart diseases, and metabolism. In mammals, six PRDX members have been identified and are subdivided into three subfamilies: typical 2-Cys (PRDX1, PRDX2, PRDX3, and PRDX4), atypical 2-Cys (PRDX5), and 1-Cys (PRDX6) subfamilies. Knockout mouse models of PRDXs have been developed to investigate their in vivo roles. This review presents an overview of the knockout mouse models of PRDXs with emphases on the biological and physiological changes of these model mice.

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Section: Discussionmentioning

confidence: 99%

“…Prdx5 deficiency leads to increased susceptibility to high-fat-diet-induced obesity, and thus Prdx5-knockout mice fed a high-fat diet show several metabolic abnormalities, including increased body weight, adipocyte hypertrophy, fat accumulation in the liver, hepatic steatosis, and an increased triglyceride level in the serum [94,96].…”

Section: Metabolismmentioning

confidence: 99%

Knockout Mouse Models for Peroxiredoxins

Lee

2020

Antioxidants

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“…In general, lipid metabolism and accumulation in hepatocytes leads to hepatic steatosis, the first step of NAFLD. NAFLD can progress to NASH, advanced hepatic fibrosis, and cirrhosis [39,40]. The present study dealt with the steatosis stage of NAFLD in an animal model.…”

Section: Discussionmentioning

confidence: 99%

Water Extract of Curcuma longa L. Ameliorates Non-Alcoholic Fatty Liver Disease

et al. 2019

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Our aim was to investigate whether hot water extract (CLW) of Curcuma longa L. could prevent non-alcoholic fatty liver disease (NAFLD). HepG2 cells were treated with free fatty acid (FFA) mixture (oleic acid: palmitic acid, 2:1) for 24 h to stimulate in vitro fatty liver. In addition, C57BL/6 mice were fed 60 kcal% high-fat (HF) diet for eight weeks to induce fatty liver in vivo. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) productions were increased by FFA and HF-diet, but supplementation with CLW significantly decreased these levels. CLW treatment ameliorated antioxidant activities that were suppressed by exposure to the FFA and HF-diet. Cluster of differentiation 36 (CD36) and fatty acid transport proteins (FATP2 and FATP5) were increased in HF-diet groups, while CLW suppressed their expression levels. Moreover, sterol regulatory element-binding protein-1c (SREBP-1c), acetyl-coenzyme A carboxylase (ACC), and fatty acid synthase (FAS) expression levels were down-regulated in the CLW groups compared to HF-diet groups. On the other hand, 5′ adenosine monophosphate-activated protein kinase (AMPK), Peroxisome proliferator-activated receptor alpha (PPAR-α), and carnitine palmitoyltransferase 1 (CPT-1) expressions were up-regulated in the CLW groups. HF-diet fed mice showed high hepatic triglycerides (TG) content compared to the normal diet mice. However, the administration of CLW restored the hepatic TG level, indicating an inhibitory effect against lipid accumulation by CLW. These results suggest that CLW could be a potentially useful agent for the prevention of NAFLD through modulating fatty acid uptake.

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“…Another study induced hepatic steatosis in a HepG2 cell line with treatment of FFA to simulate an obese state in vitro . Inducing PrxV overexpression ameliorated hepatic steatosis progression by inhibiting lipogenesis associated protein, SREBP-1 and RAS, and FFA-induced mitochondrial ROS generation ( Kim et al., 2020 ). A follow-up study in mice revealed that the mechanism of PrxV in achieving this role appears to be through phosphorylation of AMPK pathway ( Kim et al., 2020 ).…”

Section: Antioxidants In Ameliorating Obesity and Associated Comorbidmentioning

confidence: 99%

“…Inducing PrxV overexpression ameliorated hepatic steatosis progression by inhibiting lipogenesis associated protein, SREBP-1 and RAS, and FFA-induced mitochondrial ROS generation ( Kim et al., 2020 ). A follow-up study in mice revealed that the mechanism of PrxV in achieving this role appears to be through phosphorylation of AMPK pathway ( Kim et al., 2020 ). Two separate studies have also implicated PrxIV and PrxVI in having a protective role against steatosis by targeting mitochondrial ROS generation ( Yamada and Guo, 2018 ; Lee et al., 2019 ).…”

Section: Antioxidants In Ameliorating Obesity and Associated Comorbidmentioning

confidence: 99%

Therapeutic Efficacy of Antioxidants in Ameliorating Obesity Phenotype and Associated Comorbidities

et al. 2020

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Obesity has been a worldwide epidemic for decades. Despite the abundant increase in knowledge regarding the etiology and pathogenesis of obesity, the prevalence continues to rise with estimates predicting considerably higher numbers by the year 2030. Obesity is characterized by an abnormal lipid accumulation, however, the physiological consequences of obesity are far more concerning. The development of the obesity phenotype constitutes dramatic alterations in adipocytes, along with several other cellular mechanisms which causes substantial increase in systemic oxidative stress mediated by reactive oxygen species (ROS). These alterations promote a chronic state of inflammation in the body caused by the redox imbalance. Together, the systemic oxidative stress and chronic inflammation plays a vital role in maintaining the obese state and exacerbating onset of cardiovascular complications, Type II diabetes mellitus, dyslipidemia, non-alcoholic steatohepatitis, and other conditions where obesity has been linked as a significant risk factor. Because of the apparent role of oxidative stress in the pathogenesis of obesity, there has been a growing interest in attenuating the pro-oxidant state in obesity. Hence, this review aims to highlight the therapeutic role of antioxidants, agents that negate pro-oxidant state of cells, in ameliorating obesity and associated comorbidities. More specifically, this review will explore how various antioxidants target unique and diverse pathways to exhibit an antioxidant defense mechanism.

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Peroxiredoxin 5 ameliorates obesity-induced non-alcoholic fatty liver disease through the regulation of oxidative stress and AMP-activated protein kinase signaling

Cited by 60 publications

References 50 publications

Knockout Mouse Models for Peroxiredoxins

Knockout Mouse Models for Peroxiredoxins

Water Extract of Curcuma longa L. Ameliorates Non-Alcoholic Fatty Liver Disease

Therapeutic Efficacy of Antioxidants in Ameliorating Obesity Phenotype and Associated Comorbidities

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