scholarly journals Difference in Hepatic Metabolism of Long- and Medium-Chain Fatty Acids: the Role of Fatty Acid Chain Length in the Production of the Alcoholic Fatty Liver*

1967 ◽  
Vol 46 (9) ◽  
pp. 1451-1460 ◽  
Author(s):  
Charles S. Lieber ◽  
André Lefèvre ◽  
Norton Spritz ◽  
Lawrence Feinman ◽  
Leonore M. DeCarli
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Liver ◽  
Chain Length ◽  
Hepatic Metabolism ◽  
Alcoholic Fatty Liver ◽  
Medium Chain ◽  
Medium Chain Fatty Acids ◽  
Fatty Acid Chain

scholarly journals Effects of adrenaline on ketogenesis from long- and medium-chain fatty acids in starved rats

1982 ◽  
Vol 204 (3) ◽  
pp. 749-756 ◽  
Author(s):  
M C Sugden ◽  
D I Watts ◽  
C E Marshall
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Blood Glucose ◽  
Carboxylic Acid ◽  
Chain Length ◽  
Clinical Significance ◽  
Ketone Body ◽  
Medium Chain ◽  
Medium Chain Fatty Acids ◽  
Increase Blood Glucose

1. Injection of adrenaline into 24 h-starved rats caused a 69% decrease in blood [ketone-body] (3-hydroxybutyrate plus acetoacetate), accompanied by a decreased [3-hydroxybutyrate]/[acetoacetate] ratio. Blood [glucose] and [lactate] increased, but [alanine] was unchanged. 2. Adrenaline also decreased [ketone-body] after intragastric feeding of both long- and medium-chain triacylglycerol. The latter decrease was observed after suppression of lipolysis with 5-methylpyrazole-3-carboxylic acid, indicating that the antiketogenic action of adrenaline was not dependent on the chain length of the precursor fatty acid. 3. The actions of adrenaline to decrease blood [ketone-body] and to increase blood [glucose] were not observed after administration of 3-mercaptopicolinate, an inhibitor of gluconeogenesis. This suggests that these effects of the hormone are related. 4. The possible clinical significance of the results is discussed with reference to the restricted ketosis often observed after surgical or orthopaedic injury.

scholarly journals Effects of propionate and carnitine on the hepatic oxidation of short- and medium-chain-length fatty acids

1988 ◽  
Vol 250 (3) ◽  
pp. 819-825 ◽  
Author(s):  
E P Brass ◽  
R A Beyerinck
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Organic Acid ◽  
Chain Length ◽  
Ketone Body ◽  
Acetyl Coa ◽  
Body Formation ◽  
Medium Chain ◽  
Medium Chain Length ◽  
Hepatic Oxidation

Accumulation of propionate, or its metabolic product propionyl-CoA, can disrupt normal cellular metabolism. The present study examined the effects of propionate, or propionyl-CoA generated during the oxidation of odd-chain-length fatty acids, on hepatic oxidation of short- and medium-chain-length fatty acids. In isolated hepatocytes, ketone-body formation from odd-chain-length fatty acids was slow as compared with even-chain-length fatty acid substrates, and increased as the carbon chain length was increased from five to seven to nine. In contrast, rates of ketogenesis from butyrate, hexonoate and octanoate were all approximately equal. Propionate (10 mM) inhibited ketogenesis from butyrate, hexanoate and octanoate by 81%, 53% and 18% respectively. Addition of carnitine had no effect on ketogenesis from the even-chain-length fatty acids, but increased the rate of ketone-body formation from pentanoate (by 53%), heptanoate (by 28%) and from butyrate or hexanoate in the presence of propionate. The inhibitory effect of propionate could not be explained by shunting acetyl-CoA into the tricarboxylic acid cycle, as CO2 formation from butyrate was also decreased by propionate. Examination of the hepatocyte CoA pool during oxidation of butyrate demonstrated that addition of propionate decreased acetyl-CoA and CoA as propionyl-CoA accumulated. Addition of carnitine decreased propionyl-CoA by 50% (associated with production of propionylcarnitine) and increased acetyl-CoA and CoA. Similar changes in the CoA pool were seen during the oxidation of pentanoate. These results demonstrate that accumulation of propionyl-CoA results in inhibition of short-chain fatty acid oxidation. Carnitine can partially reverse this inhibition. Changes in the hepatocyte CoA pool are consistent with carnitine acting by generating propionylcarnitine, thereby decreasing propionyl-CoA and increasing availability of free CoA. The data provide further evidence of the potential cellular toxicity from organic acid accretion, and supports the concept that carnitine's interaction with the cellular CoA pool can have a beneficial effect on cellular metabolism and function under conditions of unusual organic acid accumulation.

scholarly journals Effect of storage on fatty acid profile of butter from cows fed whole or ground flaxseed with or without monensin

2010 ◽  
Vol 39 (10) ◽  
pp. 2297-2303 ◽  
Author(s):  
Daniele Cristina da Silva-Kazama ◽  
Geraldo Tadeu dos Santos ◽  
Paula Toshimi Matumoto Pintro ◽  
Jesuí Vergílio Visentainer ◽  
Ricardo Kazama ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Fatty Acid Profile ◽  
Saturated Fatty Acids ◽  
Relative Percentage ◽  
Medium Chain ◽  
Medium Chain Fatty Acids ◽  
Ground Flaxseed ◽  
Chain Fatty Acids

Eight Holstein cows with body weight 570 ± 43 kg and 60 ± 20 lactation days were distributed in a double Latin square design with four 21-day periods to determine the effects of feeding ground or whole flaxseed with or without monensin supplementation (0.02% on a dry matter basis) on fatty acid profile of butter stored for 15 and 45 days. Ground flaxseed supply, in comparison to whole flaxseed, reduced relative percentages of 16:0, cis7-16:1, 17:0, and cis10-17:1 but it increased those of cis9,trans11-18:2, cis3-18:3, and omega 3 fatty acids in butter fat, reducing relative percentage of medium-chain fatty acids and increasing the content of polyunsaturated fatty acids. Supplementation with monensin increased relative percentages of cis9,trans11-18:2 and tended to increase relative percentage of 17:0 and decrease that of saturated fatty acids in butter. Butter from cows fed diet with monensin presented lower relative percentages of cis 6-20:4. Relative percentages of cis 9-16:1, cis10-17:1, 18:0, trans11-18:1, cis9-18:1, cis3-18:3, cis6-20:4 in butter stored for 15 days were higher than those stored for 45 days and the relative percentages of cis3-20:5 tended to decrease with the increase of storage period. As a result, relative percentages of saturated fatty acids and medium-chain fatty acids increased with storage time, while those of monounsaturated and long-chain fatty acids decreased. Butter enriched with polyunsaturated fatty acids may have a shorter shelf life due to the negative effect of storage on fatty acid profile which may cause oxidation and rancidity.

Evidence that fatty acid chain length is a type II cell lipid-sorting signal

1991 ◽  
Vol 260 (2) ◽  
pp. L44-L51 ◽  
Author(s):  
K. J. Longmuir ◽  
S. Haynes
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Chain Length ◽  
Molecular Species ◽  
Palmitoleic Acid ◽  
Lamellar Body ◽  
Structural Features ◽  
Type Ii ◽  
Fatty Acid Chain ◽  
Type Ii Cell

This study was undertaken to determine those structural features of phospholipid molecules which influence their enrichment in type II cell lamellar body material. Cultured fetal rabbit lung tissue was labeled with [1-14C]acetate, type II cells were isolated, and extracellular lamellar body and microsomal fractions were prepared. Radiolabeled molecular species of phosphatidylcholine (PC) and phosphatidylethanolamine were analyzed by high-performance liquid chromatography (HPLC), followed by silver nitrate thin-layer chromatography of HPLC peak fractions that overlapped. Compared with microsomes, lamellar body PC was selectively enriched with molecular species containing 14- and 16-carbon fatty acids and depleted of species containing 18-carbon fatty acids. Palmitoleic acid and an ether linkage positively influenced the enrichment of PC molecular species in the lamellar body material, but these structural features were secondary to the predominant influence of fatty acid chain length. In vivo, lung tissue normally contains low levels of palmitoleic acid; hence most unsaturated fatty acids are 18-carbons or longer. A cellular lipid-sorting mechanism that selects PCs by recognition of 14- and 16-carbon fatty acid chains (and not by recognition of fatty acid saturation) should serve to enrich the resulting pulmonary surfactant with disaturated molecular species of PC.

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