Differential Effects of Fish Oil, Safflower Oil and Palm Oil on Fatty Acid Oxidation and Glycerolipid Synthesis in Rat Liver

1991 ◽  
Vol 121 (10) ◽  
pp. 1554-1561 ◽  
Author(s):  
Margaret A. Halminski ◽  
Julian B. Marsh ◽  
Earl H. Harrison
1989 ◽  
Vol 257 (4) ◽  
pp. R822-R828 ◽  
Author(s):  
M. J. Azain ◽  
J. A. Ontko

These studies were undertaken to further characterize and explain the differences in hepatic fatty acid metabolism between lean and obese Zucker rats. It was shown that the rate of palmitate or octanoate oxidation and the inhibition of palmitate oxidation by malonyl CoA in mitochondria isolated from lean and obese Zucker rats were similar. Cytochrome oxidase activity was similar in lean and obese rat livers. It was found that the addition of cytosol from the obese rat liver inhibited palmitate oxidation by 20-30% in mitochondria isolated from lean or obese rat livers and thus reproduced the conditions observed in the intact cell. Increased concentrations of metabolites such as malonyl CoA and glycerophosphate in the liver of the obese rat are likely contributors to this inhibitory effect. These results are extrapolated to the intact cell and suggest that decreased hepatic fatty acid oxidation in the obese rat can be accounted for by cytosolic influences on the mitochondria. The decreased rate of fatty acid oxidation observed in the intact hepatocyte or perfused liver cannot be explained by a defect in the capacity of mitochondria to oxidize substrate or by a decrease in mitochondrial number in the obese rat liver.


1981 ◽  
Vol 99 (4) ◽  
pp. 1216-1225 ◽  
Author(s):  
Nariko Kawamura ◽  
Hugo W. Moser ◽  
Yasuo Kishimoto

FEBS Letters ◽  
1992 ◽  
Vol 310 (2) ◽  
pp. 193-196 ◽  
Author(s):  
Myriam Orellana ◽  
Oscar Fuentes ◽  
Helen Rosenbluth ◽  
Mauricio Lara ◽  
Elena Valdés

1981 ◽  
Vol 200 (2) ◽  
pp. 217-223 ◽  
Author(s):  
J D McGarry ◽  
D W Foster

The experiments reconfirm the powerful inhibitory effect of malonyl-CoA on carnitine acyltransferase I and fatty acid oxidation in rat liver mitochondria (Ki 1.5 microM). Sensitivity decreased with starvation (Ki after 18 h starvation 3.0 microM, and after 42 h 5.0 microM). Observations by Cook, Otto & Cornell [Biochem. J. (1980) 192, 955--958] and Ontko & Johns [Biochem. J. (1980) 192, 959--962] have cast doubt on the physiological role of malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis. The high Ki values obtained in the cited studies are shown to be due to incubation conditions that cause substrate depletion, destruction of malonyl-CoA or generation of excessively high concentrations of unbound acyl-CoA (which offsets the competitive inhibition of malonyl-CoA towards carnitine acyltransferase I). The present results are entirely consistent with the postulated role of malonyl-CoA as the primary regulatory of fatty acid synthesis and oxidation in rat liver.


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