scholarly journals Pathophysiological Analysis of the Progression of Hepatic Lesions in STAM Mice

2017 ◽  
pp. 791-799 ◽  
Author(s):  
T. SAITO ◽  
M. MURAMATSU ◽  
Y. ISHII ◽  
Y. SAIGO ◽  
T. KONUMA ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
High Fat ◽  
Lesion Formation ◽  
Hepatic Lipid Accumulation ◽  
Current Health ◽  
Hepatic Lesions ◽  
Changes Over Time ◽  
A Current ◽  
Immunohistochemical Analyses

Nonalcoholic steatohepatitis (NASH) is a current health issue since the disease often leads to hepatocellular carcinoma; however, the pathogenesis of the disease has still not been fully elucidated. In this study, we investigated the pathophysiological changes observed in hepatic lesions in STAM mice, a novel NASH model. STAM mice, high fat-diet (HFD) fed mice, and streptozotocin (STZ) treated mice were prepared, and changes over time, such as biological parameters, mRNA expression, and histopathological findings, were evaluated once animal reached 5, 7, and 10 weeks of age. STZ mice presented with hyperglycemia and an increase in oxidative stress in immunohistochemical analyses of Hexanoyl-lysine: HEL from 5 weeks, with fibrosis in the liver also being observed from 5 weeks. HFD mice presented with hyperinsulinemia from 7 weeks and the slight hepatosteatosis was observed at 5 weeks, with changes significantly increasing until 10 weeks. STAM mice at 10 weeks showed significant hepatic changes, including hepatosteatosis, hypertrophic hepatocytes, and fibrosis, indicating pathological changes associated with NASH. These results suggested that the increase in oxidative stress with hyperglycemia triggered hepatic lesions in STAM mice, and insulin resistance promoted lesion formation with hepatic lipid accumulation. STAM mice may be a useful model for elucidating the pathogenesis of NASH with diabetes.

scholarly journals Electromagnetic Fields Ameliorate Hepatic Lipid Accumulation and Oxidative Stress by Activating the CaMKKβ/AMPK/SREBP-1c and Nrf2 Pathways in High-Fat Diet-Fed Mice

2021 ◽  
Author(s):  
Mingming Zhai ◽  
Jinxiu Cui ◽  
Chenxu Zhang ◽  
Juan Liu ◽  
Yuanzhe Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Protein Expression ◽  
Electromagnetic Fields ◽  
High Fat Diet ◽  
Lipid Deposition ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

Abstract Background: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, and is related to disturbed lipid metabolism and redox homeostasis. However, a definitive drug treatment has not been approved for this disease. Studies have found that electromagnetic fields (EMFs) can ameliorate hepatic steatosis and oxidative stress. Nevertheless, the mechanism remains unclear.Methods: NAFLD models were established by feeding mice a high-fat diet. Simultaneously, EMF exposure is performed. The effects of the EMF on hepatic lipid deposition and oxidative stress were investigated. Additionally, the AMPK and Nrf2 pathways were analysed to confirm whether they were activated by the EMF.Results: Administration of the EMF decreased the body weight, liver weight and serum triglyceride (TG) levels and restrained the excessive hepatic lipid accumulation caused by feeding the HFD. This EMF function is achieved by boosting CaMKKβ protein expression, activating AMPK phosphorylation and suppressing mature SREBP-1c protein expression. Meanwhile, the activity of GSH-Px was enhanced following an increase in nuclear Nrf2 protein expression by EMF. However, no change was observed in the activities of SOD and CAT. Consequently, EMF reduced hepatic reactive oxygen species (ROS) and MDA levels, which means that EMF relieved liver damage by oxidative stress in HFD-fed mice.Conclusions: EMF can activate the CaMKKβ/AMPK/SREBP-1c and Nrf2 pathways to control hepatic lipid deposition and oxidative stress. This investigation indicates that EMF may be a novel therapeutic method for NAFLD.

scholarly journals Optimized Rapeseed Oils Rich in Endogenous Micronutrients Protect High Fat Diet Fed Rats from Hepatic Lipid Accumulation and Oxidative Stress

Nutrients ◽  
2015 ◽  
Vol 7 (10) ◽  
pp. 8491-8502 ◽  
Author(s):  
Jiqu Xu ◽  
Xiaoli Liu ◽  
Hui Gao ◽  
Chang Chen ◽  
Qianchun Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

scholarly journals BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Jian Wang ◽  
Chi Zhang ◽  
Zhiguo Zhang ◽  
Qiang Chen ◽  
Xuemian Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Growth Factor ◽  
Liver Damage ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Liver Weight ◽  
High Fat ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

The present study was to investigate whether amagnoliaextract, named BL153, can prevent obesity-induced liver damage and identify the possible protective mechanism. To this end, obese mice were induced by feeding with high fat diet (HFD, 60% kcal as fat) and the age-matched control mice were fed with control diet (10% kcal as fat) for 6 months. Simultaneously these mice were treated with or without BL153 daily at 3 dose levels (2.5, 5, and 10 mg/kg) by gavage. HFD feeding significantly increased the body weight and the liver weight. Administration of BL153 significantly reduced the liver weight but without effects on body weight. As a critical step of the development of NAFLD, hepatic fibrosis was induced in the mice fed with HFD, shown by upregulating the expression of connective tissue growth factor and transforming growth factor beta 1, which were significantly attenuated by BL153 in a dose-dependent manner. Mechanism study revealed that BL153 significantly suppressed HFD induced hepatic lipid accumulation and oxidative stress and slightly prevented liver inflammation. These results suggest that HFD induced fibrosis in the liver can be prevented partially by BL153, probably due to reduction of hepatic lipid accumulation, inflammation and oxidative stress.

Uridine attenuates obesity, ameliorates hepatic lipid accumulation and modifies the gut microbiota composition in mice fed with a high-fat diet

2021 ◽  
Author(s):  
Yilin Liu ◽  
Chunyan Xie ◽  
Zhenya Zhai ◽  
Ze-yuan Deng ◽  
Hugo R. De Jonge ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Microbiota Composition ◽  
High Fat ◽  
Fat Accumulation ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Gut Microbiota Composition

This study aimed to investigate the effect of uridine on obesity, fat accumulation in liver, and gut microbiota composition in high-fat diet-fed mice.

Hesperetin ameliorates hepatic oxidative stress and inflammation via the PI3K/AKT-Nrf2-ARE pathway in oleic acid-induced HepG2 cells and a rat model of high-fat diet-induced NAFLD

2021 ◽  
Author(s):  
Jingda Li ◽  
Tianqi Wang ◽  
Panpan Liu ◽  
Fuyuan Yang ◽  
Xudong Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oleic Acid ◽  
Rat Model ◽  
High Fat Diet ◽  
Hepg2 Cells ◽  
Citrus Fruits ◽  
High Fat ◽  
Hepatic Oxidative Stress

Hesperetin as a major bioflavonoid in citrus fruits improves NAFLD by suppressing hepatic oxidative stress and inflammation.

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