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.

THE EFFECT OF RIMONABANT ON HEPATIC FREE FATTY ACID PROFILE IN MICE WITH NONALCOHOLIC FATTY LIVER DISEASE

2018 ◽  
Vol 25 (3) ◽  
pp. 214
Author(s):  
Bojan Jorgačević ◽  
Danijela Vučević ◽  
Ivana Djuričić ◽  
Sladjana Šobajić ◽  
Dušan Mladenović ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Free Fatty Acid ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Acid Profile ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver

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.

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.

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