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 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.

scholarly journals Changes of the Fatty Acid Profile in Erythrocyte Membranes of Patients following 6-Month Dietary Intervention Aimed at the Regression of Nonalcoholic Fatty Liver Disease (NAFLD)

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Dominika Maciejewska ◽  
Wojciech Marlicz ◽  
Karina Ryterska ◽  
Marcin Banaszczak ◽  
Dominika Jamioł-Milc ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Acid Profile ◽  
Fatty Liver Disease ◽  
Dietary Intervention ◽  
Erythrocyte Membranes ◽  
Nonalcoholic Fatty Liver

Background. Nonalcoholic fatty liver disease (NAFLD) is closely related to the metabolism disorders of fatty acids. The pathogenesis of the disease includes an increased concentration of FFA in blood, an increase in the biosynthesis of fatty acids, and disorders in the process of β-oxidation. Objective. The aim of the study was to analyze the fatty acids in erythrocyte membranes among 55 patients with NAFLD who were subjected to a 6-month dietary intervention in order to reduce fatty liver. Materials and Methods. Basic anthropometric and biochemical measurements were performed. The profile of fatty acids was measured in the membranes of erythrocytes and analyzed by gas chromatography. The dietary compliance was evaluated using 72-diary questionnaires, anthropometric measurements. Results. With the reduction of fatty liver (p<0.01), the patients’ biochemical and anthropometric parameters were significantly improved. A significant decrease in the concentration of alanine aminotransferase (p<0.01) and asparagine aminotransferase (p<0.01) was observed, along with a decrease in the amount of insulin (p<0.05) and insulin resistance (p<0.05). Significant changes in terms of the fatty acid profile were observed among patients who followed the dietary intervention. There was a noticeable tendency in terms of the reduction palmitic acid (p<0.055) and a significant reduction of stearic acid (p<0.05). Significant changes in the profile of fatty acids were also associated with the reductionof palmitoleic (p<0.05) and oleic acids (p<0.05). Another statistically significant change observed was the increase in polyunsaturated fatty acids. In particular (p<0.01) the rise of eicosapentaenoic (p<0.055) and docosahexaenoic acids (p<0.55) was noted. Conclusion. The profile of fatty acids turned out to be a potential biomarker of the liver changes during NAFLD regression. Further research is needed to fully elucidate the usefulness and applicability of our findings in the management of NAFLD.

scholarly journals Metabolic and Genetic Determinants of Lipid Metabolism Disruption in Non-Alcoholic Fatty Liver Disease

2020 ◽  
Vol 30 (2) ◽  
pp. 15-25
Author(s):  
O. Yu. Kytikova ◽  
T. P. Novgorodtseva ◽  
Yu. K. Denisenko ◽  
D. A. Kovalevsky
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Fatty Acid Desaturases ◽  
Alcoholic Fatty Liver ◽  
Genetic Mechanisms ◽  
Alcoholic Fatty Liver Disease

Aim. To present literature data on the metabolic and genetic mechanisms of impaired fatty acid (FA) synthesis in the development and progression of non-alcoholic fatty liver disease (NAFLD).General findings. NAFLD is a widespread disease progressing from steatosis to non-alcoholic steatohepatitis (NASH), increasing the risk of cirrhosis, liver failure and hepatocellular carcinoma. Progression of NAFLD and the development of NASH are closely related to lipid metabolism disorders caused not only by insufficient alimentary intake of fatty acids, but also by a decrease in the efficiency of their endogenous processing. The regulation of fatty acid metabolism involves enzymes desaturase (FADS1, FADS2) and elongase (ELOVL2 and ELOVL5) fatty acids. Desaturases are encoded by the FADS1 and FADS2 genes for fatty acid desaturases. Polymorphisms in the genes of fatty acid desaturases determine the effectiveness of PUFA endogenous processing. Violations in the activity of FADS1 and FADS2 and their genes are accompanied by dysregulation of the metabolic pathway involved in the biosynthesis of fatty acids. This leads to the damage of cell membranes, whose main components are represented by phospholipids. The progression of NAFLD is associated with the powerful toxicity of lipids released in the liver parenchyma upon the loss of the cell biomembrane integrity.Conclusions. Further research into the NAFLD genetic mechanisms regulating the metabolism of fatty acids appears to be promising for a deeper understanding of the pathogenesis of this multifactorial disease.

scholarly journals Simple and facilitated diffusion of long chain fatty acids in the pathogenesis of nonalcoholic fatty liver disease

2017 ◽  
Vol 71 (0) ◽  
pp. 0-0 ◽  
Author(s):  
Klaudia Berk ◽  
Nicoletta Iłowska ◽  
Karolina Konstantynowicz-Nowicka ◽  
Adrian Chabowski
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Facilitated Diffusion ◽  
Long Chain Fatty Acids ◽  
Nonalcoholic Fatty Liver ◽  
Long Chain

Nonalcoholic fatty liver disease (NAFLD) is defined as lipid accumulation in hepatocytes, in the absence of alcohol use, that exceeds 5% of liver size. The most frequent comorbidities of NAFLD include diabetes mellitus, insulin resistance and hyperlipidemia. The accumulation of various lipid fractions results from excessive hepatic uptake of long chain fatty acids (LCFA) that is not compensated by oxidation. The cellular influx of LCFA occurs in the mechanism of passive diffusion through fenestrations in sinusoidal endothelium, and is due to caveolae system which participates in the endocytosis of macromolecules. The dynamic character of fenestration and their changes caused by the application of a different dietary pattern may indicate that they contribute to the development of metabolic disturbances. The second way of the LCFA entrance to the cells is through a facilitated transport that involves fatty acid transporters: translocase FAT/CD36, fatty acid binding protein FABPpm, fatty acid transport proteins FATP2 and FATP5, which are localized in the cell. It has been proven that changes in the expression of these transporters are strongly associated with abnormal lipid metabolism in the liver. The key aim of this review is to describe the possible ways of intracellular lipid uptake to the liver in terms of NAFLD development and accompanying obesity. The role of facilitated diffusion, being necessary for the efficient function of the liver, is also presented.

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