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.
Analytical, anthropometric and dietary factors associated with the development of fibrosis in patients with nonalcoholic fatty liver disease
