Membrane Binding Proteins are the Major Determinants for the Hepatocellular Transmembrane Flux of Long-Chain Fatty Acids Bound to Albumin

2005 ◽  
Vol 22 (11) ◽  
pp. 1793-1804 ◽  
Author(s):  
G. Rajaraman ◽  
M. S. Roberts ◽  
D. Hung ◽  
G. Q. Wang ◽  
F. J. Burczynski
Keyword(s):  
Fatty Acids ◽  
Binding Proteins ◽  
Membrane Binding ◽  
Long Chain Fatty Acids ◽  
Transmembrane Flux ◽  
Long Chain ◽  
Chain Fatty Acids

Is there facilitated uptake of fatty acids by the liver? Interpretation and analysis of experimental data

1995 ◽  
Vol 73 (4) ◽  
pp. 409-420 ◽  
Author(s):  
F. J. Burczynski ◽  
B. A. Luxon
Keyword(s):  
Experimental Data ◽  
Fatty Acids ◽  
Binding Proteins ◽  
Serum Proteins ◽  
Fluid Layer ◽  
Organic Anion ◽  
Long Chain Fatty Acids ◽  
Uptake Mechanism ◽  
Long Chain ◽  
Chain Fatty Acids

Uptake of hydrophobic organic anions that are extensively bound to serum proteins has been a controversial issue for over 30 years. It is known that steady-state uptake is lower in the presence of binding proteins, but it is much higher than predicted on the basis of protein–ligand binding equilibrium. Several theories have been postulated to account for this observation. Recent work has shown how binding proteins are capable of enhancing the uptake rate of long-chain fatty acids by decreasing the diffusional resistance of the unstirred fluid layer. The enhanced transport via codiffusion is especially important for tightly bound ligands like long-chain fatty acids. Whether this model accounts for all experimental data or whether hepatocytes facilitate the uptake of protein-bound ligands, by for example mediating the protein–ligand dissociation rate, is not clear. We review the published reports to gain an understanding into the potential mechanism for the extraction of long-chain fatty acids. Understanding the uptake mechanism of these important metabolic substrates is vitally important in determining their overall utilization in a variety of clinical disorders as diverse as gallstones, obesity, and atherosclerosis.Key words: surface charge, pI, albumin, lysozyme, orosmucoid, α1-acid glycoprotein, protein binding, palmitate, organic anion, uptake, hepatocytes, facilitation, diffusion, unstirred fluid layer, myocytes, long-chain fatty acids, fatty acids.

scholarly journals Differential Effects of Fatty Acid Saturation and Chain Length on NASH in Juvenile Iberian Pigs

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 682-682 ◽  
Author(s):  
Kayla Dillard ◽  
Morgan Coffin ◽  
Gabriella Hernandez ◽  
Victoria Smith ◽  
Catherine Johnson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Fatty Acid ◽  
Liver Injury ◽  
Olive Oil ◽  
Coconut Oil ◽  
Long Chain Fatty Acids ◽  
Medium Chain ◽  
Long Chain ◽  
Chain Fatty Acids

Abstract Objectives Non-alcoholic fatty liver disease (NAFLD) represents the major cause of pediatric chronic liver pathology in the United States. The objective of this study was to compare the relative effect of inclusion of isocaloric amounts of saturated medium-chain fatty acids (hydrogenated coconut oil), saturated long-chain fatty acids (lard) and unsaturated long-chain fatty acids (olive oil) on endpoints of NAFLD and insulin resistance. Methods Thirty-eight 15-d-old Iberian pigs were fed 1 of 4 diets containing (g/kg body weight × d) 1) control (CON; n = 8): 0 g fructose, 10.5 g fat, and 187 kcal metabolizable energy (ME), 2) lard (LAR; n = 10): 21.6 g fructose, 17.1 g fat (100% lard) and 299 kcal ME, 3) hydrogenated coconut oil (COCO; n = 10): 21.6 g fructose, 16.9 g fat (42.5% lard and 57.5% coconut oil) and 299 kcal ME, and 4) olive oil (OLV, n = 10): 21.6 g fructose, 17.1 g fat (43.5% lard and 56.5% olive oil) and 299 kcal ME, for 9 consecutive weeks. Body weight was recorded every 3 d. Serum markers of liver injury and dyslipidemia were measured on d 60 at 2 h post feeding, with all other serum measures assessed on d 70. Liver tissue was collected on d 70 for histology, triacylglyceride (TG) quantification, and metabolomics analysis. Results Tissue histology indicated the presence of steatosis in LAR, COCO and OLV compared with CON (P ≤ 0.001), with a further increase in in non-alcoholic steatohepatitis (NASH) in OLV and COCO compared with LAR (P ≤ 0.01). Alanine and aspartate aminotransferases were higher in COCO and OLV (P ≤ 0.01) than CON. All treatment groups had lower liver concentrations of methyl donor's choline and betaine versus CON, while bile acids were differentially changed (P ≤ 0.05). COCO had higher levels of TGs with less carbons (Total carbons < 52) than all other groups (P ≤ 0.05). Several long-chain acylcarnitines involved in fat oxidation were higher in OLV versus all other groups (P ≤ 0.05). Conclusions Inclusion of fats enriched in medium-chain saturated and long-chain unsaturated fatty acids in a high-fructose high-fat diet increased liver injury, compared with fats with a long-chain saturated fatty acid profile. Further research is required to investigate the mechanisms causing this difference in physiological response to these dietary fat sources. Funding Sources ARI, AcornSeekers.

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