Altered fatty acid metabolism and reduced stearoyl-coenzyme a desaturase activity in asthma

Allergy ◽  
2017 ◽  
Vol 72 (11) ◽  
pp. 1744-1752 ◽  
Author(s):  
N. Rodriguez-Perez ◽  
E. Schiavi ◽  
R. Frei ◽  
R. Ferstl ◽  
P. Wawrzyniak ◽  
...  
1989 ◽  
Vol 256 (1) ◽  
pp. E31-E38 ◽  
Author(s):  
N. Takeyama ◽  
D. Takagi ◽  
N. Matsuo ◽  
Y. Kitazawa ◽  
T. Tanaka

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.


2013 ◽  
Vol 33 (9) ◽  
pp. 1869-1882 ◽  
Author(s):  
Jessica M. Ellis ◽  
G. William Wong ◽  
Michael J. Wolfgang

Numerous neurological diseases are associated with dysregulated lipid metabolism; however, the basic metabolic control of fatty acid metabolism in neurons remains enigmatic. Here we have shown that neurons have abundant expression and activity of the long-chain cytoplasmic acyl coenzyme A (acyl-CoA) thioesterase 7 (ACOT7) to regulate lipid retention and metabolism. Unbiased and targeted metabolomic analysis of fasted mice with a conditional knockout of ACOT7 in the nervous system, Acot7 N−/− , revealed increased fatty acid flux into multiple long-chain acyl-CoA-dependent pathways. The alterations in brain fatty acid metabolism were concomitant with a loss of lean mass, hypermetabolism, hepatic steatosis, dyslipidemia, and behavioral hyperexcitability in Acot7 N − / − mice. These failures in adaptive energy metabolism are common in neurodegenerative diseases. In agreement, Acot7 N − / − mice exhibit neurological dysfunction and neurodegeneration. These data show that ACOT7 counterregulates fatty acid metabolism in neurons and protects against neurotoxicity.


1956 ◽  
Vol 222 (2) ◽  
pp. 795-802
Author(s):  
RoscoeO. Brady ◽  
Abdel-Megid Mamoon ◽  
E.R. Stadtman

2014 ◽  
Vol 192 (7) ◽  
pp. 3190-3199 ◽  
Author(s):  
JangEun Lee ◽  
Matthew C. Walsh ◽  
Kyle L. Hoehn ◽  
David E. James ◽  
E. John Wherry ◽  
...  

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