scholarly journals Black Sesame Seeds Ethanol Extract Ameliorates Hepatic Lipid Accumulation, Oxidative Stress, and Insulin Resistance in Fructose-Induced Nonalcoholic Fatty Liver Disease

2018 ◽  
Vol 66 (40) ◽  
pp. 10458-10469 ◽  
Author(s):  
Yang Yang ◽  
Jingjing Wang ◽  
Yongmin Zhang ◽  
Jing Li ◽  
Wenji Sun
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Ethanol Extract ◽  
Nonalcoholic Fatty Liver ◽  
Sesame Seeds ◽  
Hepatic Lipid Accumulation

scholarly journals Isoquercetin Improves Hepatic Lipid Accumulation by Activating AMPK Pathway and Suppressing TGF-β Signaling on an HFD-Induced Nonalcoholic Fatty Liver Disease Rat Model

2018 ◽  
Vol 19 (12) ◽  
pp. 4126 ◽  
Author(s):  
Guohong Qin ◽  
Ji Ma ◽  
Qiongshan Huang ◽  
Hongli Yin ◽  
Jichun Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Kupffer Cells ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid Accumulation ◽  
Ampk Pathway ◽  
And Oxidative Stress

Isoquercetin (IQ), a glucoside derivative of quercetin, has been reported to have beneficial effects in nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the potential improvement of IQ in liver lipid accumulation, inflammation, oxidative condition, and activation in Kupffer cells (KCs) on a high-fat diet (HFD) induced NAFLD models. Male Sprague-Dawley (SD) rats were induced by HFD, lipopolysaccharides/free fatty acids (LPS/FFA) induced co-culture cells model between primary hepatocytes and Kupffer cells was used to test the effects and the underlying mechanism of IQ. Molecular docking was performed to predict the potential target of IQ. Significant effects of IQ were found on reduced lipid accumulation, inflammation, and oxidative stress. In addition, AMP-activated protein kinase (AMPK) pathway was activated by IQ, and is plays an important role in lipid regulation. Meanwhile, IQ reversed the increase of activated KCs which caused by lipid overload, and also suppression of Transforming growth factor beta (TGF-β) signaling by TGF-β Recptor-1 and SMAD2/3 signaling. Finally, TGF-βR1 and TGF-βR2 were both found may involve in the mechanism of IQ. IQ can improve hepatic lipid accumulation and decrease inflammation and oxidative stress by its activating AMPK pathway and suppressing TGF-β signaling to alleviate NAFLD.

scholarly journals Understanding the Role of Exercise in Nonalcoholic Fatty Liver Disease: ERS-Linked Molecular Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Yong Zou ◽  
Zhengtang Qi
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Molecular Pathways ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Nonalcoholic fatty liver disease (NAFLD) is globally prevalent and characterized by abnormal lipid accumulation in the liver, frequently accompanied by insulin resistance (IR), enhanced hepatic inflammation, and apoptosis. Recent studies showed that endoplasmic reticulum stress (ERS) at the subcellular level underlies these featured pathologies in the development of NAFLD. As an effective treatment, exercise significantly reduces hepatic lipid accumulation and thus alleviates NAFLD. Confusingly, these benefits of exercise are associated with increased or decreased ERS in the liver. Further, the interaction between diet, medication, exercise types, and intensity in ERS regulation is more confusing, though most studies have confirmed the benefits of exercise. In this review, we focus on understanding the role of exercise-modulated ERS in NAFLD and ERS-linked molecular pathways. Moderate ERS is an essential signaling for hepatic lipid homeostasis. Higher ERS may lead to increased inflammation and apoptosis in the liver, while lower ERS may lead to the accumulation of misfolded proteins. Therefore, exercise acts like an igniter or extinguisher to keep ERS at an appropriate level by turning it up or down, which depends on diet, medications, exercise intensity, etc. Exercise not only enhances hepatic tolerance to ERS but also prevents the malignant development of steatosis due to excessive ERS.

Effect of black garlic on visceral fat, oxidative stress and insulin resistance in nonalcoholic fatty liver disease rats

2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Alifia Mukti Fajrani ◽  
Mohamad Sulchan ◽  
Siti Fatimah Muis ◽  
Hery Djagat Purnomo ◽  
Kis Djamiatun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Liver Disease ◽  
Vitamin E ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Visceral Fat ◽  
Fatty Liver Disease ◽  
Content Type ◽  
Nonalcoholic Fatty Liver

Purpose This paper aims to determine the effect of black garlic (BG) on visceral fat, oxidative stress and insulin resistance (IR) compared with metformin and vitamin E in nonalcoholic fatty liver disease (NAFLD) rats. Design/methodology/approach A randomized post-test only design with control group was used in this study. Rats were given high-fat fructose diet enriched with 1.25% cholesterol and 0.5% cholic acid for eight weeks to induce NALFD condition. The administration of BG dose of 450 mg/200 gBW, 900 mg/200 gBW and 1350 mg/200 gBW with a comparative control of 45 mg/200 gBW of metformin and vitamin E of 9 IU/200 gBW were given for four weeks via oral gavage to reduce visceral fat, oxidative stress and improve IR. Statistical analyses were performed to examine differences between groups with one-way analysis of variance and nonparametrics test. Findings Rats given with three different doses of BG for four weeks did not reduce body weight from 244 ± 4.4 to 284 ± 4.6 g, 242 ± 2.5 to 272 ± 3.1 g and 240 ± 2.4 to 270 ± 3.6 g, respectively, but significantly reduced visceral fat (p = 0.001) on BG groups with 3.7 ± 1.3, 2.7 ± 0.7 and 1.8 ± 0.6 g, respectively. BG improved oxidative stress (p = 0.001) with malondialdehyde level 5.1 ± 0.2, 3.0 ± 0.06 and 2.3 ± 0.06 ng/mL, respectively, but did not better than vitamin E group 1 ± 0.03 ng/mL. Significant (p = 0.001) improvement on insulin resistance with homeostatic model assessment IR in BG groups were 5.3 ± 0.1, 4.4 ± 0.1 and 4 ± 0.1, respectively, but not as good as metformin group 3.7 ± 0.1. Research limitations/implications Based on the experiment, there are several limitations including small sample size, performed on animal models in a relatively short time, did not examine organosulfurs compound (OSC) content of BG specifically and OSC affects metabolism in NAFLD remains unclear and will require further investigation. Practical implications BG is a functional food made from heated fresh garlic owing to the Maillard reaction and the organosulfur compounds as antioxidants. The higher the dose of BG, the greater the improvement in visceral fat, oxidative stress and IR in model NAFLD rats. Social implications NAFLD is a liver disorder caused by excessive fat and energy intake, the treatment strategies among others through diet modification. Originality/value In model NAFLD rats, BG administration improved NALFD markers but did not better rather than the metformin and vitamin E result.

Simultaneous co-assembly of fenofibrate and ketoprofen peptide for the dual-targeted treatment of nonalcoholic fatty liver disease (NAFLD)

2020 ◽  
Vol 56 (36) ◽  
pp. 4922-4925 ◽  
Author(s):  
Zhongyan Wang ◽  
Chuanrui Ma ◽  
Yuna Shang ◽  
Lijun Yang ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Inflammatory Responses ◽  
Targeted Treatment ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

An ingenious co-assembled nanosystem based on fenofibrate and ketoprofen peptide for the dual-targeted treatment of NAFLD by reducing hepatic lipid accumulation and inflammatory responses.

scholarly journals Macrovesicular steatosis in nonalcoholic fatty liver disease is a consequence of purine nucleotide cycle driven fumarate accumulation

2020 ◽  
Author(s):  
Matthew C. Sinton ◽  
Baltasar Lucendo Villarin ◽  
Jose Meseguer Ripolles ◽  
Sara Wernig-Zorc ◽  
John P. Thomson ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Purine Nucleotide ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Purine Nucleotide Cycle

SummaryNonalcoholic fatty liver disease (NAFLD) affects ~88% of obese individuals and is characterised by hepatic lipid accumulation. Mitochondrial metabolic dysfunction is a feature of NAFLD. We used a human pluripotent stem cell-based system to determine how mitochondrial dysfunction is linked to hepatic lipid accumulation. We induced lipid accumulation in hepatocyte-like cells (HLCs) using lactate, pyruvate and octanoate (LPO). Transcriptomic analysis revealed perturbation of mitochondrial respiratory pathways in LPO exposed cells. Using 13C isotopic tracing, we identified truncation of the TCA cycle in steatotic HLCs. We show that increased purine nucleotide cycle (PNC) activity fuels fumarate accumulation and drives lipid accumulation in steatotic cells. These findings provide new insights into the pathogenesis of hepatic steatosis and may lead to an improved understanding of the metabolic and transcriptional rewiring associated with NAFLD.

Ginsenoside CK ameliorates hepatic lipid accumulation via activating LKB1/AMPK pathway in vitro and in vivo

2022 ◽  
Author(s):  
Jingjing Zhang ◽  
Xiaoxuan Ma ◽  
Daidi Fan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid Accumulation

Nonalcoholic fatty liver disease (NAFLD) is a metabolic liver disease with complex etiology, which is considered as one of the main causes of hepatocellular carcinoma (HCC). The incidence of NAFLD...

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