Simple and facilitated diffusion of long chain fatty acids in the pathogenesis of nonalcoholic fatty liver disease
Journal Title: Advances in Hygiene and Experimental Medicine - Year 2017, Vol 71, Issue
Abstract
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.
Authors and Affiliations
Klaudia Berk, Nicoletta Iłowska, Karolina Konstantynowicz-Nowicka, Adrian Chabowski
Keywords
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- EP ID EP248479
- DOI 10.5604/01.3001.0010.7668
- Views 139
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