scholarly journals Biochemical aspects associated with an ethanol-induced fatty liver

1970 ◽  
Vol 119 (3) ◽  
pp. 511-516 ◽  
Author(s):  
Jennifer E. C. Walker ◽  
Ellen R. Gordon
Keyword(s):  
Fatty Liver ◽  
Adenosine Triphosphatase ◽  
Control Diet ◽  
Fatty Infiltration ◽  
Caloric Intake ◽  
Liver Homogenate ◽  
Liver Glycogen ◽  
Hepatic Triglyceride ◽  
Triglyceride Content ◽  
Increased Activity

Isocaloric replacement of either the fat or carbohydrate content of the diet by ethanol (36% of the total caloric intake) produced fatty infiltration of the liver in rats. The increase in hepatic triglyceride content was associated with a decrease in both ATP and glycogen contents. Increased activity of mitochondrial Mg2+-stimulated adenosine triphosphatase paralleled the increase in the free Pi content of the liver homogenate. During the regression of the fatty liver, glycogen contents returned to normal within 24h of the removal of ethanol from the diet. Not until the third day after the withdrawal of ethanol had the Mg2+-stimulated adenosine triphosphatase activity and free Pi content of the homogenate returned to normal. A slow regression of the triglyceride content from the liver occurred and by the fifth day both ATP and triglyceride concentrations had returned to the values observed in the rats given the liquid control diet.

scholarly journals Effects of Ethanol Feeding in Early-Stage NAFLD Mice Induced by Western Diet

Livers ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 27-39
Author(s):  
Maximilian Joseph Brol ◽  
Stella Georgiou ◽  
Ditlev Nytoft Rasmussen ◽  
Cristina Ortiz ◽  
Sabine Klein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Early Stage ◽  
Western Diet ◽  
Hepatic Triglyceride ◽  
Expression Levels ◽  
Triglyceride Content ◽  
Gene Expression Levels

Background: The prevalence of metabolic liver diseases is increasing and approved pharmacological treatments are still missing. Many animal models of nonalcoholic fatty liver disease (NAFLD) show a full spectrum of fibrosis, inflammation and steatosis, which does not reflect the human situation since only up to one third of the patients develop fibrosis and nonalcoholic steatohepatitis (NASH). Methods: Seven week old C57Bl/J mice were treated with ethanol, Western diet (WD) or both. The animals’ liver phenotypes were determined through histology, immunohistochemistry, Western blotting, hepatic triglyceride content and gene expression levels. In a human cohort of 80 patients stratified by current alcohol misuse and body mass index, liver histology and gene expression analysis were performed. Results: WD diet and ethanol-treated animals showed severe steatosis, with high hepatic triglyceride content and upregulation of fatty acid synthesis. Mild fibrosis was revealed using Sirius-red stains and gene expression levels of collagen. Inflammation was detected using histology, immunohistochemistry and upregulation of proinflammatory genes. The human cohort of obese drinkers showed similar upregulation in genes related to steatosis, fibrosis and inflammation. Conclusions: We provide a novel murine model for early-stage fatty liver disease suitable for drug testing and investigation of pathophysiology.

Effect of Chinese Herbal Monomer Hairy Calycosin on Nonalcoholic Fatty Liver Rats and its Mechanism

2019 ◽  
Vol 22 (3) ◽  
pp. 194-200 ◽  
Author(s):  
Xiang Liu ◽  
Zhi-Hong Xie ◽  
Chen-Yuan Liu ◽  
Ying Zhang
Keyword(s):  
Fatty Liver ◽  
Liver Tissue ◽  
Liver Homogenate ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Alcoholic Fatty Liver ◽  
Nonalcoholic Fatty Liver ◽  
Chinese Herbal ◽  
Tnf Α ◽  
Model Control

Background: Chinese herbal monomer hairy Calycosin is a flavonoid extracted from Radix astragali. Aims and Scope: The aim of the research was to investigate the effect and mechanism of Hairy Calycosin on Non-Alcoholic Fatty Liver Dieases (NAFLD) in rats. Materials and Methods: 60 rats were randomly divided into 6 groups, then NAFLD rat models were prepared and treated with different doses of Hairy Calycosin (0.5, 1.0, 2.0 mg/kg) or Kathyle relatively. Results: Both 1.0 mg/kg and 2.0 mg/kg Hairy Calycosin treatment could significantly increase the serum Superoxide Dismutase (SOD) content of the model rats and reduce the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), Free Fatty Acid (FFA), IL-6, tumor necrosis factor-alpha (TNF-α) and liver homogenate malondialdehyde (MDA), while 2.0 mg/kg Hairy Calycosin can down-regulate liver tissue cytochrome p450 2E1 (CYP2E1). In the electron microscope, compared with the model control group, the mitochondrial swelling in the hepatocytes of Hairy Calycosin (1.0, 2.0 mg/kg) treatment group was significantly reduced, the ridge on the inner membrane of mitochondria increased, and the lipid droplets became much smaller. Conclusion: Hairy Calycosin can effectively control the lipid peroxidation in liver tissues of rats with NAFLD, and reduce the levels of serum TNF-α, IL-6, MDA and FFA, effectively improve the steatosis and inflammation of liver tissue, and down-regulate the expression of CYP2E1, inhibit apoptosis of hepatocytes.

Anti-obesity Effect of Gold Nanoparticles from Dendropanax morbifera Léveille by Suppression of Triglyceride Synthesis and Downregulation of PPARγ and CEBPα Signaling Pathways in 3T3-L1 Mature Adipocytes and HepG2 Cells

2020 ◽  
Vol 16 (2) ◽  
pp. 196-203 ◽  
Author(s):  
Myoung Hi Yi ◽  
Shakina Yesmin Simu ◽  
Sungeun Ahn ◽  
Verónica Castro Aceituno ◽  
Chao Wang ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Cellular Level ◽  
Dendropanax Morbifera ◽  
Immunoblotting Assay ◽  
Triglyceride Content ◽  
20 Nm ◽  
Proliferation Assays

Background: Biosynthesis of gold nanoparticles from medicinal plants has become an interesting strategy in biomedical research due to its exclusive properties including less toxic cellular level through its ecofriendly biological function. Objective: To examine the anti-lipid accumulation effect of spherical gold nanoparticles (size 10-20 nm) synthesized from Dendropanax morbifera Léveille (D-AuNPs) in both 3T3-L1 and HepG2 cells. Method: 3T3-L1 preadipocytes and HepG2 hepatocytes were stimulated with cocktail media to generate obese and fatty liver disease models. Cell cytotoxicity and cell proliferation assays were performed in adipocytes at different stages of growth. An anti-lipid accumulation assay was performed in 3T3-L1 obese and HepG2 fatty liver models using different doses of D-AuNPs. Expression of adipogenic genes of PPARγ, CEBPα, Jak2, STAT3, and ap2 and hepatogenic genes PPARα, FAS, and ACC was measured by real-time PCR. In addition, protein expression of PPARγ and CEBPα was evaluated by immunoblotting assay. Result: We found that D-AuNPs (size 10–20 nm) at concentrations up to 100 µg/ml were nontoxic to 3T3-L1 and HepG2 at post-confluent and mature stages. In addition, pretreatment of D-AuNPs at post-confluent stage reduced triglyceride content. In addition, the adipogenesis process was negatively controlled by D-AuNPs, with downregulated PPARγ, CEBPα, Jak2, STAT3, and ap2 expression in 3T3-L1 cells and FAS and ACC levels in HepG2 cells. Conclusion: These data indicated that D-AuNPs exert antiadipogenic properties. We hypothesize that Dendropanax contains a large amount of phenolic compound that coats the surface of gold nanoparticles and has the ability to reduce the excess amount of lipid in both cell lines.

Dietary raffinose ameliorates hepatic lipid accumulation induced by cholic acid via modulation of enterohepatic bile acid circulation in rats

2021 ◽  
pp. 1-26
Author(s):  
Kenta Maegawa ◽  
Haruka Koyama ◽  
Satoru Fukiya ◽  
Atsushi Yokota ◽  
Koichiro Ueda ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Bile Acid ◽  
Cholic Acid ◽  
Lipid Accumulation ◽  
Enterohepatic Circulation ◽  
Control Diet ◽  
Hepatic Triglyceride ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Abstract Enterohepatic circulation of 12α-hydroxylated (12αOH) bile acid (BA) is enhanced depending on the energy intake in high-fat diet-fed rats. Such BA metabolism can be reproduced using a diet supplemented with cholic acid (CA), which also induces simple steatosis, without inflammation and fibrosis, accompanied by some other symptoms that are frequently observed in the condition of non-alcoholic fatty liver in rats. We investigated whether supplementation of the diet with raffinose (Raf) improves hepatic lipid accumulation induced by the CA-fed condition in rats. After acclimation to the AIN-93-based control diet, male Wistar rats were fed diets supplemented with a combination of Raf (30 g/kg diet) and/or CA (0.5 g/kg diet) for 4 weeks. Dietary Raf normalised hepatic triglyceride levels (two-way ANOVA P<0.001 for CA, P=0.02 for Raf, and P=0.004 for interaction) in the CA-supplemented diet-fed rats. Dietary Raf supplementation reduced hepatic 12αOH BA concentration (two-way ANOVA P<0.001 for CA, P=0.003 for Raf, and P=0.03 for interaction). The concentration of 12αOH BA was reduced in the aortic and portal plasma. Raf supplementation increased acetic acid concentration in the caecal contents (two-way ANOVA P=0.001 as a main effect). Multiple regression analysis revealed that concentrations of aortic 12αOH BA and caecal acetic acid could serve as predictors of hepatic triglyceride concentration (R2=0.55, P<0.001). However, Raf did not decrease the secondary 12αOH BA concentration in the caecal contents as well as the transaminase activity in the CA diet-fed rats. These results imply that dietary Raf normalises hepatic lipid accumulation via suppression of enterohepatic 12αOH BA circulation.

scholarly journals RIPK3 acts as a lipid metabolism regulator contributing to inflammation and carcinogenesis in non-alcoholic fatty liver disease

Gut ◽  
2020 ◽  
pp. gutjnl-2020-321767
Author(s):  
Marta B Afonso ◽  
Pedro M Rodrigues ◽  
Miguel Mateus-Pinheiro ◽  
André L Simão ◽  
Maria M Gaspar ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Body Weight Gain ◽  
Control Diet ◽  
Peroxisome Proliferator ◽  
Functional Link ◽  
Alcoholic Fatty Liver ◽  
The Impact ◽  
Alcoholic Fatty Liver Disease

ObjectiveReceptor-interacting protein kinase 3 (RIPK3) is a key player in necroptosis execution and an emerging metabolic regulator, whose contribution to non-alcoholic fatty liver disease (NAFLD) is controversial. We aimed to clarify the impact of RIPK3 signalling in the pathogenesis of human and experimental NAFLD.DesignRIPK3 levels were evaluated in two large independent cohorts of patients with biopsy proven NAFLD diagnosis and correlated with clinical and biochemical parameters. Wild-type (WT) or Ripk3-deficient (Ripk3−/−) mice were fed a choline-deficient L-amino acid-defined diet (CDAA) or an isocaloric control diet for 32 and 66 weeks.ResultsRIPK3 increased in patients with non-alcoholic steatohepatitis (NASH) in both cohorts, correlating with hepatic inflammation and fibrosis. Accordingly, Ripk3 deficiency ameliorated CDAA-induced inflammation and fibrosis in mice at both 32 and 66 weeks. WT mice on the CDAA diet for 66 weeks developed preneoplastic nodules and displayed increased hepatocellular proliferation, which were reduced in Ripk3−/− mice. Furthermore, Ripk3 deficiency hampered tumourigenesis. Intriguingly, Ripk3−/− mice displayed increased body weight gain, while lipidomics showed that deletion of Ripk3 shifted hepatic lipid profiles. Peroxisome proliferator-activated receptor γ (PPARγ) was increased in Ripk3−/− mice and negatively correlated with hepatic RIPK3 in patients with NAFLD. Mechanistic studies established a functional link between RIPK3 and PPARγ in controlling fat deposition and fibrosis.ConclusionHepatic RIPK3 correlates with NAFLD severity in humans and mice, playing a key role in managing liver metabolism, damage, inflammation, fibrosis and carcinogenesis. Targeting RIPK3 and its intricate signalling arises as a novel promising approach to treat NASH and arrest disease progression.

scholarly journals High Dietary Glucose Intake Increases Hepatic Triglyceride Content and Oxidative Stress: Contributions of Angiotensin Receptor

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Priscilla Montez ◽  
Thorwald A. Max ◽  
Ruben Rodriguez ◽  
Jose Viscarra ◽  
José Pablo Vázquez-Medina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Receptor ◽  
Hepatic Triglyceride ◽  
Glucose Intake ◽  
Triglyceride Content ◽  
And Oxidative Stress

scholarly journals Maternal Choline Supplementation Supports Resistance to Effects of Prolonged Western Diet Feeding in Mice Offspring

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1022-1022
Author(s):  
Hunter Korsmo ◽  
Moshe Dembitzer ◽  
Sarah Khaldi ◽  
Shameera Sheeraz ◽  
Juliet Kosichenko ◽  
...  
Keyword(s):  
Maternal Obesity ◽  
De Novo ◽  
Control Diet ◽  
Caloric Intake ◽  
Metabolic Stress ◽  
Acid Synthesis ◽  
Female Offspring ◽  
Western Diet ◽  
High Fat ◽  
Glucose Levels

Abstract Objectives This study investigated whether maternal choline supplementation (MCS) could reduce the chronic metabolic stress that is induced by prenatal maternal obesity and postnatal Western Diet (WD) feeding. Methods C57BL/6 dams were either fed a normal fat (NF, 10 kcal %fat) control diet or a high fat (HF, 45 kcal % fat) diet prior to, during pregnancy and during lactation. These dams received either 25 mM choline or plain drinking water. After weaning, offspring were fed the WD diet (45 kcal %fat, 34 kcal %fructose, and 0.25% cholesterol) for 16 weeks before glucose tolerance testing and dissection. Results After 16 weeks of WD feeding, offspring from normal-fat, choline supplemented fed (MCS-NF) dams are protected from weight gain compared to offspring from dams fed a high-fat diet with or without choline supplementation (MCS-HF or MCO-HF)(P &lt; 0.043). Male offspring from MCS-NF fed dams have reduced caloric intake (P &lt; 0.019) and reduced gene expression of Acc1 which mediates liver de novo fatty acid synthesis (P = 0.005) compared to the non-supplemented normal-fat dams (MCO-NF) after 16 weeks of WD feeding. Female offspring from MCS-HF fed dams have lower fasting glucose levels compared to MCO-HF fed dams after 16 weeks of WD feeding (P = 0.034). Conclusions MCS mitigates some pathological hallmarks that are induced by prolonged WD feeding in offspring. Funding Sources NIGMS.

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