Sa1709 Decreased Lysosomal Function Impairs Autophagosome-Lysosome System in a Dietary Mice Model of Non-Alcoholic Fatty Liver Disease

2014 ◽  
Vol 146 (5) ◽  
pp. S-956
Author(s):  
Xiaojuan Wang ◽  
William K. Wu ◽  
Xiang Zhang ◽  
Eagle SH Chu ◽  
Wei Kang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Mice Model ◽  
Alcoholic Fatty Liver ◽  
Lysosomal Function ◽  
Alcoholic Fatty Liver Disease

scholarly journals Antrodan Alleviates High-Fat and High-Fructose Diet-Induced Fatty Liver Disease in C57BL/6 Mice Model via AMPK/Sirt1/SREBP-1c/PPARγ Pathway

2020 ◽  
Vol 21 (1) ◽  
pp. 360 ◽  
Author(s):  
Charng-Cherng Chyau ◽  
Hsueh-Fang Wang ◽  
Wen-Juan Zhang ◽  
Chin-Chu Chen ◽  
Shiau-Huei Huang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Mice Model ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
High Fructose Diet ◽  
High Fructose ◽  
Ant Control ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) and -steatohepatitis (NASH) imply a state of excessive fat built-up in livers with/or without inflammation and have led to serious medical concerns in recent years. Antrodan (Ant), a purified β-glucan from A. cinnamomea has been shown to exhibit tremendous bioactivity, including hepatoprotective, antihyperlipidemic, antiliver cancer, and anti-inflammatory effects. Considering the already well-known alleviating bioactivity of A. cinnamomea for the alcoholic steatohepatitis (ASH), we propose that Ant can be beneficial to NAFLD, and that the AMPK/Sirt1/PPARγ/SREBP-1c pathways may be involved in such alleviations. To uncover this, we carried out this study with 60 male C57BL/6 mice fed high-fat high-fructose diet (HFD) for 60 days, in order to induce NAFLD/NASH. Mice were then grouped and treated (by oral administration) as: G1: control; G2: HFD (HFD control); G3: Ant, 40 mgkg (Ant control); G4: HFD+Orlistat (10 mg/kg) (as Orlistat control); G5: HFD+Ant L (20 mg/kg); and G6: HFD+Ant H (40 mg/kg) for 45 days. The results indicated Ant at 40 mg/kg effectively suppressed the plasma levels of malondialdehyde, total cholesterol, triglycerides, GOT, GPT, uric acid, glucose, and insulin; upregulated leptin, adiponectin, pAMPK, Sirt1, and down-regulated PPARγ and SREBP-1c. Conclusively, Ant effectively alleviates NAFLD via AMPK/Sirt1/CREBP-1c/PPARγ pathway.

High-content hydrogen water-induced downregulation of miR-136 alleviates non-alcoholic fatty liver disease by regulating Nrf2 via targeting MEG3

2018 ◽  
Vol 399 (4) ◽  
pp. 397-406 ◽  
Author(s):  
Xiang Wang ◽  
Jiao Wang
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Cellular Model ◽  
Mice Model ◽  
Alcoholic Fatty Liver ◽  
Expression Levels ◽  
Hydrogen Water ◽  
Qrt Pcr ◽  
Alcoholic Fatty Liver Disease

AbstractThis study was aimed to investigate the potential regulatory mechanism of high-content hydrogen water (HHW) in non-alcoholic fatty liver disease (NAFLD). A high-fat diet (HFD)-induced NAFLD mice model and cellular model were prepared. The serum levels of alanine transaminase (ALT), aspartate transaminase (AST), total cholesterol (TCH) and triglycerides (TG) were measured. The expression levels of representative five microRNA (miRNAs) (miR-103, miR-488, miR-136, miR-505 and miR-148a) in liver tissues were determined by quantitative real-time PCR (qRT-PCR). The target of miR-136 was validated by RNA immunoprecipitation (RIP) and pull-down assay. MiR-136, MEG3 and nuclear factor erythroid 2-related factor 2 (Nrf2) expression levels following cell treatment were detected in hepatocytes using qRT-PCR and Western blotting. Moreover, cell viability and TG content were conducted. MiR-136 was downregulated, MEG3 as well as Nrf2 was upregulated and serum lipid level was reduced in NAFLD mice model after HHW treatment, which exerted the same effect in cellular model. RIP and RNA pull-down assay confirmed that MEG2 was a downstream target of miR-136. What’s more, HHW ameliorated lipid accumulation by regulating miR-136/MEG3/Nrf2 axisin vitroandin vivo. Hence, HHW alleviated NAFLD by downregulation of miR-136 through mediating Nrf2 via targeting MEG3.

Vanillic Acid and Non-Alcoholic Fatty Liver Disease: A Focus on AMPK in Adipose and Liver Tissues

2021 ◽  
Vol 27 ◽  
Author(s):  
Sepideh Shekari ◽  
Fatemeh Khonsha ◽  
Mohammad Rahmati-Yamchi ◽  
Hamid Reza Nejabati ◽  
Ali Mota
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Vanillic Acid ◽  
Fatty Liver Disease ◽  
Wide Spectrum ◽  
Special Focus ◽  
Protective Effects ◽  
Mice Model ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

: Non-alcoholic fatty liver disease (NAFLD), a growing health issue around the world, is defined as the presence of steatosis in the liver without any other detectable byproducts such as alcohol consumption which includes a wide spectrum of pathologies, such as steatohepatitis, cirrhosis, and hepatocellular carcinoma. A growing body of evidence indicates that the reduction in the 5' adenosine monophosphate-activated protein kinase (AMPK) activity, which could be activated by the consumption of the drugs, hormones, cytokines, and dietary restriction, is related to some metabolic disorders such as obesity, diabetes, PCOS, and NAFLD. Vanillic acid (VA), as an anti-inflammatory, anti-oxidative, anti-angiogenic and anti-metastatic factor, has protective effects on the liver as in two animal models of liver damage. It reduces serum levels of transaminases, inflammatory cytokines, and the accumulation of collagen in the liver and prevents liver fibrosis. Besides, it decreases body and adipose tissue weight in a mice model of obesity and, similar to the liver tissue, diminishes adipogenesis through the activation of AMPK. It has been reported that VA can target almost all of the metabolic abnormalities of NAFLD, such as hepatic steatosis, inflammation, and hepatic injury, at least partially through the activation of AMPK. Therefore, in this review, we will discuss the possible and hypothetical roles of VA in NAFLD, with a special focus on AMPK.

Adipogenic changes of hepatocytes in a high-fat diet-induced fatty liver mice model and non-alcoholic fatty liver disease patients

Endocrine ◽  
2014 ◽  
Vol 48 (3) ◽  
pp. 834-847 ◽  
Author(s):  
Xiaoli Pan ◽  
Pei Wang ◽  
Jinzhuo Luo ◽  
Zhijun Wang ◽  
Yuhu Song ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Mice Model ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Coffee and Intestinal Permeability in a Mice Model of Non-Alcoholic Fatty Liver Disease

2016 ◽  
Vol 64 (2) ◽  
pp. S688-S689
Author(s):  
G. Mazzone ◽  
V. Lembo ◽  
G. D’Argenio ◽  
P. Vitaglione ◽  
A. Rossi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Intestinal Permeability ◽  
Fatty Liver Disease ◽  
Mice Model ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Vitamin D levels are not associated with non-alcoholic fatty liver disease severity in a Brazilian population

2020 ◽  
pp. 1-8
Author(s):  
Jeniffer Danielle M. Dutra ◽  
Quelson Coelho Lisboa ◽  
Silvia Marinho Ferolla ◽  
Carolina Martinelli M. L. Carvalho ◽  
Camila Costa M. Mendes ◽  
...  
Keyword(s):  
Vitamin D ◽  
Liver Disease ◽  
Fatty Liver ◽  
Disease Severity ◽  
Fatty Liver Disease ◽  
Hypovitaminosis D ◽  
Alcoholic Fatty Liver ◽  
Vitamin D Levels ◽  
The Mean ◽  
Alcoholic Fatty Liver Disease

Abstract. Some epidemiological evidence suggests an inverse correlation between non-alcoholic fatty liver disease (NAFLD) frequency and vitamin D levels. Likewise, a beneficial effect of vitamin D on diabetes mellitus (DM) and insulin resistance has been observed, but this is an unsolved issue. Thus, we aimed to investigate the prevalence of hypovitaminosis D in a NAFLD Brazilian population and its association with disease severity and presence of comorbidities. In a cross-sectional study, the clinical, biochemical and histological parameters of 139 NAFLD patients were evaluated according to two different cut-off points of serum 25-hydroxyvitamin D levels (20 ng/mL and 30 ng/mL). The mean age of the population was 56 ± 16 years, most patients were female (83%), 72% had hypertension, 88% dyslipidemia, 46% DM, 98% central obesity, and 82% metabolic syndrome. Serum vitamin D levels were < 30 ng/mL in 78% of the patients, and < 20 ng/mL in 35%. The mean vitamin D level was 24.3 ± 6.8 ng/mL. The comparison between the clinical, biochemical and histological characteristics of the patients according to the levels of vitamin D showed no significant difference. Most patients with NAFLD had hypovitaminosis D, but low vitamin D levels were not related to disease severity and the presence of comorbidities.

Non-Alcoholic Fatty Liver Disease in Overweight Children and its Relationship with Retinol Serum Levels

2008 ◽  
Vol 78 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Suano de Souza ◽  
Silverio Amancio ◽  
Saccardo Sarni ◽  
Sacchi Pitta ◽  
Fernandes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Lipid Profile ◽  
Fatty Liver Disease ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Objectives: To evaluate the frequency of non-alcoholic fatty liver disease, the retinol serum levels, lipid profile, and insulin resistance in overweight/obese children. To relate these biochemical variables with the risk of this disease in the population studied. Methods: The study was cross-sectional and prospective, with 46 overweight/obese school children (28 female, 18 male; mean age 8.6 years). The control group consisted of 45 children, paired by age and gender. Hepatic steatosis, evaluated by ultrasound, was classified as normal, mild, moderate, or severe. Also evaluated were serum retinol levels; thiobarbituric acid reactive substances; lipid profile; and fasting glucose and serum insulin levels, used for the calculation of the Homeostasis Model Assessment. Results: Hepatic ultrasound alterations were found in 56.5% and 48,9% of the overweight/obese and control group children, respectively. Presence of obesity was associated with high levels of triglycerides (OR = 4.6; P = 0.002). In the studied children, the risk of steatosis was related to a trend to a higher percentage of retinol inadequacy (OR = 2.8; p = 0.051); there was no association with thiobarbituric acid reactive substances, lipid profile, or insulin resistance. Conclusions: The high frequency of non-alcoholic fatty liver disease in both groups, evaluated by hepatic ultrasound, in low-socioeconomic level children, independent of nutritional condition and without significant association with insulin resistance, emphasizes that especially in developing countries, other risk factors such as micronutrient deficiencies (e.g. vitamin A) are involved.

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