Nonalcoholic fatty liver disease: Roles of the gut and the liver and metabolic modulation by some dietary factors and especially long-chain n-3 PUFA

2015 ◽  
Vol 60 (1) ◽  
pp. 147-159 ◽  
Author(s):  
Jacques Delarue ◽  
Jean-Paul Lallès
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Dietary Factors ◽  
Nonalcoholic Fatty Liver ◽  
Metabolic Modulation ◽  
Long Chain

The therapeutic potential of long-chain omega-3 fatty acids in nonalcoholic fatty liver disease

2011 ◽  
Vol 30 (1) ◽  
pp. 6-19 ◽  
Author(s):  
Haim Shapiro ◽  
Miryam Tehilla ◽  
Joelle Attal-Singer ◽  
Rafael Bruck ◽  
Rachel Luzzatti ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Therapeutic Potential ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Nonalcoholic Fatty Liver ◽  
Long Chain

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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