scholarly journals Specific inactivation of hepatic fatty acid hydroxylases by acetylenic fatty acids.

1984 ◽  
Vol 259 (7) ◽  
pp. 4136-4141 ◽  
Author(s):  
P R Ortiz de Montellano ◽  
N O Reich
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Hepatic Fatty Acid ◽  
Acetylenic Fatty Acids

Altered hepatic fatty acid metabolism in endotoxicosis: effect of L-carnitine on survival

1989 ◽  
Vol 256 (1) ◽  
pp. E31-E38 ◽  
Author(s):  
N. Takeyama ◽  
D. Takagi ◽  
N. Matsuo ◽  
Y. Kitazawa ◽  
T. Tanaka
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Coenzyme A ◽  
Ketone Bodies ◽  
Oxidation Treatment ◽  
Hepatic Fatty Acid ◽  
Malonyl Coa ◽  
Carnitine Derivatives

The activities of palmitoyl-coenzyme A (CoA) synthetase, carnitine acetyltransferase (CAT), and carnitine palmitoyltransferase (CPT) and the levels of ketone bodies, reduced coenzyme A (CoASH), carnitine, and their esters, which are involved in fatty acid metabolism, in rat liver and plasma were measured after the administration of Escherichia coli lipopolysaccharide (LPS). We also studied the effect of L-carnitine treatment before LPS administration on survival and on hepatic fatty acid metabolism. The activities of CAT and CPT and the concentrations of ketone bodies, CoA, and carnitine derivatives (except for malonyl-CoA) declined in the liver after LPS administration. The activity of palmitoyl-CoA synthetase was changed little after LPS administration, and the level of hepatic malonyl-CoA increased significantly, suggesting that LPS causes activated fatty acids to undergo esterification and lipogenesis rather than oxidation. Treatment of rats with L-carnitine before LPS greatly increased the survival rate, but did not affect enzymes that metabolize fatty acids, CoA, or carnitine derivatives in the liver. Further studies are necessary to elucidate the mechanism of the effect of carnitine on post-LPS survival.

scholarly journals Diversity of Δ12 Fatty Acid Desaturases in Santalaceae and Their Role in Production of Seed Oil Acetylenic Fatty Acids

2013 ◽  
Vol 288 (45) ◽  
pp. 32405-32413 ◽  
Author(s):  
Shoko Okada ◽  
Xue-Rong Zhou ◽  
Katherine Damcevski ◽  
Nerida Gibb ◽  
Craig Wood ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Seed Oil ◽  
Fatty Acid Desaturases ◽  
Acetylenic Fatty Acids

scholarly journals Hepatic Fatty Acid Balance and Hepatic Fat Content in Humans With Severe Obesity

2019 ◽  
Vol 104 (12) ◽  
pp. 6171-6181 ◽  
Author(s):  
Kelli A Lytle ◽  
Nikki C Bush ◽  
Jessica M Triay ◽  
Todd A Kellogg ◽  
Michael L Kendrick ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Liver ◽  
Severe Obesity ◽  
Acid Oxidation ◽  
Hepatic Fatty Acid ◽  
Triglyceride Secretion ◽  
Hepatic Fatty Acid Oxidation ◽  
Vldl Triglyceride ◽  
Secretion Rates

Abstract Objective Nonalcoholic fatty liver disease can lead to hepatic inflammation/damage. Understanding the physiological mechanisms that contribute to excess hepatic lipid accumulation may help identify effective treatments. Design We recruited 25 nondiabetic patients with severe obesity scheduled for bariatric surgery. To evaluate liver export of triglyceride fatty acids, we measured very-low-density lipoprotein (VLDL)–triglyceride secretion rates the day prior to surgery using an infusion of autologous [1-14C]triolein-labeled VLDL particles. Ketone body response to fasting and intrahepatic long-chain acylcarnitine concentrations were used as indices of hepatic fatty acid oxidation. We measured intraoperative hepatic uptake rates of plasma free fatty acids using a continuous infusion of [U-13C]palmitate, combined with a bolus dose of [9,10-3H]palmitate and carefully timed liver biopsies. Total intrahepatic lipids were measured in liver biopsy samples to determine fatty liver status. The hepatic concentrations and enrichment from [U-13C]palmitate in diacylglycerols, sphingolipids, and acyl-carnitines were measured using liquid chromatography/tandem mass spectrometry. Results Among study participants with fatty liver disease, intrahepatic lipid was negatively correlated with VLDL-triglyceride secretion rates (r = −0.92, P = 0.01) but unrelated to hepatic free fatty acid uptake or indices of hepatic fatty acid oxidation. VLDL-triglyceride secretion rates were positively correlated with hepatic concentrations of saturated diacylglycerol (r = 0.46, P = 0.02) and sphingosine-1-phosphate (r = 0.44, P = 0.03). Conclusion We conclude that in nondiabetic humans with severe obesity, excess intrahepatic lipid is associated with limited export of triglyceride in VLDL particles rather than increased uptake of systemic free fatty acids.

Recognition of Fatty Acids by Hepatic Fatty Acid Binding Proteins

1986 ◽  
Vol 88 (S2) ◽  
pp. 588-592 ◽  
Author(s):  
U. Bordewick ◽  
H. Schulenberg ◽  
P. Schäfer ◽  
F. Spener
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Binding Proteins ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding ◽  
Hepatic Fatty Acid

scholarly journals Zonation of hepatic fat accumulation: insights from mathematical modelling of nutrient gradients and fatty acid uptake

2017 ◽  
Vol 14 (133) ◽  
pp. 20170443 ◽  
Author(s):  
Jana Schleicher ◽  
Uta Dahmen ◽  
Reinhard Guthke ◽  
Stefan Schuster
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Theoretical Perspective ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Maximal Velocity ◽  
Uptake Mechanism ◽  
Alcoholic Fatty Liver ◽  
Hepatic Fatty Acid ◽  
Triglyceride Accumulation

Intrinsic of non-alcoholic fatty liver diseases is an aberrant accumulation of triglycerides (steatosis), which occurs inhomogeneously within lobules. To improve our understanding of the mechanisms involved in this zonation patterning, we developed a mathematical multicompartment model of hepatic fatty acid metabolism accompanied by blood flow simulations. A model analysis determines the influence of the uptake process of fatty acids, the porto-central gradient of plasma fatty acid concentration, and the oxygen supply via blood on the zonation of triglyceride accumulation. From this theoretical perspective, the plasma oxygen gradient, but not the fatty acid gradient, leads the way to a zonated triglyceride accumulation by its decisive role in oxidative processes. In addition, the uptake mechanism of fatty acids seems to be fundamental for a pericentral dominance of steatosis. However, the mechanism of cellular fatty acid uptake from the blood is still under debate. Our theoretical approach supports the transporter-mediated uptake mechanism and reveals that the maximal velocity of fatty acid uptake affects the switching between a periportal and a pericentral triglyceride accumulation. Further research on hepatic fatty acid uptake is needed to push forward our understanding of aberrant triglyceride accumulation in diet-induced steatosis.

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