Docosahexaenoic Acid PreventsTrans-10,Cis-12–Conjugated Linoleic Acid-Induced Nonalcoholic Fatty Liver Disease in Mice by Altering Expression of Hepatic Genes Regulating Fatty Acid Synthesis and Oxidation

2012 ◽  
Vol 10 (3) ◽  
pp. 175-180 ◽  
Author(s):  
Dawn M. Fedor ◽  
Yuriko Adkins ◽  
Bruce E. Mackey ◽  
Darshan S. Kelley
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Linoleic Acid ◽  
Docosahexaenoic Acid ◽  
Fatty Liver ◽  
Fatty Acid Synthesis ◽  
Fatty Liver Disease ◽  
Acid Synthesis ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Genes

scholarly journals Acetyl-CoA carboxylase inhibition by ND-630 reduces hepatic steatosis, improves insulin sensitivity, and modulates dyslipidemia in rats

2016 ◽  
Vol 113 (13) ◽  
pp. E1796-E1805 ◽  
Author(s):  
Geraldine Harriman ◽  
Jeremy Greenwood ◽  
Sathesh Bhat ◽  
Xinyi Huang ◽  
Ruiying Wang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Fatty Acid Synthesis ◽  
Fatty Liver Disease ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
Acetyl Coa Carboxylase

Simultaneous inhibition of the acetyl-CoA carboxylase (ACC) isozymes ACC1 and ACC2 results in concomitant inhibition of fatty acid synthesis and stimulation of fatty acid oxidation and may favorably affect the morbidity and mortality associated with obesity, diabetes, and fatty liver disease. Using structure-based drug design, we have identified a series of potent allosteric protein–protein interaction inhibitors, exemplified by ND-630, that interact within the ACC phosphopeptide acceptor and dimerization site to prevent dimerization and inhibit the enzymatic activity of both ACC isozymes, reduce fatty acid synthesis and stimulate fatty acid oxidation in cultured cells and in animals, and exhibit favorable drug-like properties. When administered chronically to rats with diet-induced obesity, ND-630 reduces hepatic steatosis, improves insulin sensitivity, reduces weight gain without affecting food intake, and favorably affects dyslipidemia. When administered chronically to Zucker diabetic fatty rats, ND-630 reduces hepatic steatosis, improves glucose-stimulated insulin secretion, and reduces hemoglobin A1c (0.9% reduction). Together, these data suggest that ACC inhibition by representatives of this series may be useful in treating a variety of metabolic disorders, including metabolic syndrome, type 2 diabetes mellitus, and fatty liver disease.

scholarly journals Red Quinoa Bran Extract Prevented Alcoholic Fatty Liver Disease via Increasing Antioxidative System and Repressing Fatty Acid Synthesis Factors in Mice Fed Alcohol Liquid Diet

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6973
Author(s):  
Ting-An Lin ◽  
Bo-Jun Ke ◽  
Shih-Cheng Cheng ◽  
Chun-Lin Lee
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Liver Injury ◽  
Fatty Liver ◽  
Fatty Acid Synthesis ◽  
Fatty Liver Disease ◽  
Acid Synthesis ◽  
Alcoholic Fatty Liver ◽  
Ethanol Extraction ◽  
Alcoholic Fatty Liver Disease

Alcohol is metabolized in liver. Chronic alcohol abuse results in alcohol-induced fatty liver and liver injury. Red quinoa (Chenopodium formosanum) was a traditional staple food for Taiwanese aborigines. Red quinoa bran (RQB) included strong anti-oxidative and anti-inflammatory polyphenolic compounds, but it was usually regarded as the agricultural waste. Therefore, this study is to investigate the effect of water and ethanol extraction products of RQB on the prevention of liquid alcoholic diet-induced acute liver injury in mice. The mice were given whole grain powder of red quinoa (RQ-P), RQB ethanol extract (RQB-E), RQB water extract (RQB-W), and rutin orally for 6 weeks, respectively. The results indicated that RQB-E, RQB-W, and rutin decreased alcoholic diet-induced activities of aspartate aminotransferase and alanine aminotransferase, and the levels of serum triglyceride, total cholesterol, and hepatic triglyceride. Hematoxylin and eosin staining of liver tissues showed that RQB-E and RQB-W reduced lipid droplet accumulation and liver injury. However, ethanol extraction process can gain high rutin and antioxidative agents contents from red quinoa, that showed strong effects in preventing alcoholic fatty liver disease and liver injury via increasing superoxide dismutase/catalase antioxidative system and repressing the expressions of fatty acid synthesis enzyme acetyl-CoA carboxylase.

Nano Biotechnology Investigation of the Fatty Acid Synthesis (FAS): Preventing the Fatty Liver Disease

2017 ◽  
Vol 14 (1) ◽  
pp. 659-669
Author(s):  
Arina Rahimi ◽  
Majid Monajjemi
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Liver Disease ◽  
Electrical Properties ◽  
Potential Energy ◽  
Fatty Liver ◽  
Computational Chemistry ◽  
Fatty Acid Synthesis ◽  
Fatty Liver Disease ◽  
Acid Synthesis

Fatty acids in liver are subject to different patterns of regulation and the importance of fat deposition began to be realized with the evolution of vertebrates and the liver was the initial site of deposition. Modern sharks frequently have massive livers containing cells loaded with triglycerides. Based on our previous works we have modeled and simulated various molecules of those fatty acids. A number of computational chemistry studies carried out to understand the of the fatty acid synthesis (FAS) for preventing the fatty liver disease. In this work the electrical properties such as electron densities, energy densities, potential energy densities, ELF, LOL, ellipticity of electron density, eta index and ECP for some of the fatty acids have been calculated.

scholarly journals Role of Docosahexaenoic Acid Treatment in Improving Liver Histology in Pediatric Nonalcoholic Fatty Liver Disease

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e88005 ◽  
Author(s):  
Valerio Nobili ◽  
Guido Carpino ◽  
Anna Alisi ◽  
Rita De Vito ◽  
Antonio Franchitto ◽  
...  
Keyword(s):  
Liver Disease ◽  
Docosahexaenoic Acid ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Acid Treatment ◽  
Liver Histology ◽  
Nonalcoholic Fatty Liver

scholarly journals Diospyros kaki and Citrus unshiu Mixture Improves Disorders of Lipid Metabolism in Nonalcoholic Fatty Liver Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Mi-Rae Shin ◽  
Sung Ho Shin ◽  
Seong-Soo Roh
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Fatty Acid Synthase ◽  
Diospyros Kaki ◽  
Citrus Unshiu ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) has been a major cause of a chronic liver disease over recent decades and increasing worldwide in parallel with the remarkable growth of obesity. In the present study, we investigate the ameliorative effects of PCM, a combination of Diospyros kaki fruit and Citrus unshiu peel mixture, on high-fat diet- (HFD-) induced NAFLD and clarify the potential mechanisms. PCM in HFD-fed mice was orally administered at a dose of 50 or 100 mg/kg subsequently for 2 months. Thereafter, lipid metabolism parameters and fat synthesis-related genes in the mouse liver were evaluated. Subsequently, body weight changes, liver weight, serum liver function and lipid profiles, and liver pathology were examined, and the relative levels of fatty acid synthesis and β-oxidation gene expression were evaluated by western blot. Serum AST, ALT, and TG levels in the HFD control mice were significantly higher than those of normal mice. Compared with HFD control mice, PCM supplementation increased phosphorylation of AMP-activated protein kinase (AMPK). Peroxisome proliferator-activated receptor (PPAR) α was significantly increased by PCM administration. Continuously, the activation of PPARα significantly elevated carnitine palmitoyltransferase 1 (CPT-1), a key enzyme in fatty acid β-oxidation, and mitochondrial uncoupling protein 2 (UCP-2), thermogenic regulatory genes, in PCM-treated mice compared with those of HFD control mice. Moreover, PCM inhibits lipogenesis and cholesterol synthesis via suppression of sterol regulatory element binding protein-1 (SREBP-1) and SREBP-2 and its target genes such as acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). Taken together, these effects were mediated through activation of AMPK. In the conclusion, PCM improved liver damage in HFD-fed mice and attenuated NAFLD by the activation of PPARα and the inhibition of SREBPs expression via AMPK-dependent pathways.

scholarly journals Estimation of Fish and ω-3 Fatty Acid Intake in Pediatric Nonalcoholic Fatty Liver Disease

2013 ◽  
Vol 57 (5) ◽  
pp. 627-633 ◽  
Author(s):  
David E. St-Jules ◽  
Corilee A. Watters ◽  
Elizabeth M. Brunt ◽  
Lynne R. Wilkens ◽  
Rachel Novotny ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Fatty Acid Intake ◽  
Nonalcoholic Fatty Liver ◽  
Acid Intake

1282 CHARACTERISTICS OF THE FATTY ACID COMPOSITION IN NONALCOHOLIC FATTY LIVER DISEASE (NAFLD)

2011 ◽  
Vol 54 ◽  
pp. S505-S506
Author(s):  
K. Yamada ◽  
E. Mizukoshi ◽  
Y. Takeshita ◽  
K. Arai ◽  
T. Yamashita ◽  
...  
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Acid Composition ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver
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