scholarly journals Altered interactions between lipogenesis and fatty acid oxidation in regenerating rat liver

1987 ◽  
Vol 241 (2) ◽  
pp. 469-474 ◽  
Author(s):  
P S Schofield ◽  
M C Sugden ◽  
C G Corstorphine ◽  
V A Zammit
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Ketone Bodies ◽  
Tricarboxylic Acid Cycle ◽  
Acid Oxidation ◽  
Regenerating Liver ◽  
Liver Remnant ◽  
Malonyl Coa ◽  
Blood Ketone Bodies ◽  
Long Chain

The concentrations of malonyl-CoA, citrate, ketone bodies and long-chain acylcarnitine were measured in freeze-clamped liver samples from fed or starved normal, partially hepatectomized or sham-operated rats. These parameters were used in conjunction with measurements of the concentration of plasma non-esterified fatty acids and the rates of hepatic lipogenesis to obtain correlations between rates of fatty acid delivery to the liver, lipogenesis and fatty acid oxidation to ketone bodies and CO2. These correlations indicated that the development of fatty liver after partial hepatectomy is due to an increased partitioning of long-chain acyl-CoA towards acylglycerol synthesis and away from acylcarnitine formation. However, this did not appear to be due to an altered relationship between hepatic malonyl-CoA concentration and acylcarnitine formation. For any concentration of long-chain acylcarnitine, the concentrations of both hepatic and blood ketone bodies were significantly lower in partially hepatectomized rats than in normal or sham-operated animals. This indicated that a lower proportion of the product of beta-oxidation was used for ketone-body formation and more for citrate synthesis in the regenerating liver, especially during the first 24 h after resection. This inference was supported by the changes in hepatic citrate concentrations observed. The high rates of lipogenesis that occurred in the liver remnant were accompanied by an altered relationship between lipogenic rate and hepatic malonyl-CoA concentration, such that much lower concentrations of malonyl-CoA were associated with any given rate of lipogenesis. These adaptations are discussed in relation to the requirements by the remnant for high rates of energy formation through the tricarboxylic acid cycle during the first 24 h after resection, and the possibility that cycling between fatty acid oxidation and synthesis may occur to a greater degree in regenerating liver.

scholarly journals The effects of inhibition of fatty acid oxidation in suckling newborn rats

1977 ◽  
Vol 166 (3) ◽  
pp. 631-634 ◽  
Author(s):  
J P Pégorier ◽  
P Ferré ◽  
J Girard
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Fatty Acid Oxidation ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Normal Blood ◽  
Acid Oxidation ◽  
Newborn Rats ◽  
Normal Blood Glucose ◽  
Blood Ketone Bodies

Inhibition of fatty acid oxidation with pent-4-enoate in suckling newborn rats caused a fall in blood [glucose] and blood [ketone bodies] and inhibition of gluconeogenesis from lactate. Glucose utilization was not increased in newborn rats injected with pent-4-enoate. Active fatty acid oxidation appears to be essential to support gluconeogenesis and to maintain normal blood [glucose] in suckling newborn rats.

Parenteral and enteral metabolism of anaplerotic triheptanoin in normal rats

2006 ◽  
Vol 291 (4) ◽  
pp. E860-E866 ◽  
Author(s):  
Renée P. Kinman ◽  
Takhar Kasumov ◽  
Kathryn A. Jobbins ◽  
Katherine R. Thomas ◽  
Jillian E. Adams ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Ketone Bodies ◽  
Chain Fatty Acid ◽  
Acid Oxidation ◽  
Inherited Disorders ◽  
Long Chain Fatty Acid ◽  
Peripheral Tissues ◽  
Caloric Requirement ◽  
Long Chain

A new chronic treatment for inherited disorders of long-chain fatty acid oxidation involves administering up to one-third of dietary calories as triheptanoin, a medium-odd-chain triglyceride (Roe CR, Sweetman L, Roe DS, David F, and Brunengraber H. J Clin Invest 110: 259–269, 2002). Heptanoate and C5-ketone bodies derived from its partial oxidation in liver are precursors of anaplerotic propionyl-CoA in peripheral tissues. It was hypothesized that increasing anaplerosis in peripheral tissues would boost energy production. In the present study, we tested the potential of a triheptanoin emulsion as an intravenous nutrient. Normal rats were infused with triheptanoin intravenously or intraduodenally at up to 40% of caloric requirement. The blood concentration ratio (heptanoate/C5-ketone bodies) was high with intravenous and low with intraduodenal triheptanoin infusion. During intravenous infusion of triheptanoin, lipolysis was stimulated but appeared compensated by fatty acid reesterification. During intraduodenal infusion of triheptanoin, lipolysis was not stimulated. Our data support the hypothesis that intravenous triheptanoin could be used to treat decompensated patients with long-chain fatty acid oxidation disorders.

scholarly journals Evaluation of malonyl-CoA in the regulation of long-chain fatty acid oxidation in the liver. Evidence for an unidentified regulatory component of the system

1980 ◽  
Vol 192 (3) ◽  
pp. 959-962 ◽  
Author(s):  
J A Ontko ◽  
M L Johns
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Liver Mitochondria ◽  
Chain Fatty Acid ◽  
Molar Ratio ◽  
Acid Oxidation ◽  
Long Chain Fatty Acid ◽  
Malonyl Coa ◽  
Site Of Action ◽  
Long Chain

Palmitate oxidation by liver mitochondria from fed and starved rats exhibited markedly different sensitivities to inhibition by malonyl-CoA. In the mitochondrial system from fed rats, 50% inhibition required 19 muM-malonyl-CoA, whereas the mitochondria from starved rats were by comparison refractory to malonyl-CoA. Inhibition by malonyl-CoA was completely reversed by increasing the molar ratio of fatty acid to albumin. Results indicate that the potential effectiveness of malonyl-CoA as an inhibitor of fatty acid oxidation in the liver is dependent on an unidentified regulatory component of the system. The functional activity of this component is modified by the nutritional state, and its site of action is at the mitochondrial level.

An explanation for decreased ketogenesis in the liver of the obese Zucker rat

1989 ◽  
Vol 257 (4) ◽  
pp. R822-R828 ◽  
Author(s):  
M. J. Azain ◽  
J. A. Ontko
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Rat Liver ◽  
Intact Cell ◽  
Zucker Rats ◽  
Acid Oxidation ◽  
Palmitate Oxidation ◽  
Malonyl Coa ◽  
Obese Zucker Rats ◽  
Rat Livers

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.

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