scholarly journals Effects of milk diets containing beef tallow or coconut oil on the fatty acid metabolism of liver slices from preruminant calves

2000 ◽  
Vol 84 (3) ◽  
pp. 309-318 ◽  
Author(s):  
Benoît Graulet ◽  
Dominique Gruffat-Mouty ◽  
Denys Durand ◽  
Dominique Bauchart
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Beef Tallow ◽  
Neutral Lipids ◽  
Lipid Production ◽  
Coconut Oil ◽  
Acid Oxidation ◽  
Milk Diet ◽  
Liver Slices ◽  
Triacylglycerol Accumulation

Coconut oil (CO) induces a triacylglycerol infiltration in the hepatocytes of preruminant calves when given as the sole source of fat in the milk diet over a long-term period. Metabolic pathways potentially involved in this hepatic triacylglycerol accumulation were studied by in vitro methods on liver slices from preruminant Holstein × Friesian male calves fed a conventional milk diet containing CO (n 5) or beef tallow (BT, n 5) for 19 d. Liver slices were incubated for 12 h in the presence of 0·8 mM-[14C] oleate or -[14C] laurate added to the medium. Fatty acid oxidation was determined by measuring the production of CO2 (total oxidation) and acid-soluble products (partial oxidation). Production of CO2 was 1·7–3·6-fold lower (P 0·0490) and production of acid-soluble products tended to be lower (P = 0·0625) in liver slices of CO- than BT-fed calves. Fatty acid esterification as neutral lipids was 2·6– to 3·1–fold higher (P = 0·0088) in liver slices prepared from calves fed the CO diet compared with calves fed the BT diet. By contrast with what occurs in the liver of rats fed CO, the increase in neutral lipid production did not stimulate VLDL secretion by the hepatocytes of calves fed with CO, leading to a triacylglycerol accumulation in the cytosol. It could be explained by the reduction of fatty acid oxidation favouring esterification in the form of triacylglycerols, in association with a limited availability of triacylglycerols and/or apolipoprotein B for VLDL packaging and subsequent secretion.

Studies on the control of fatty acid oxidation in liver preparations from chick embryos

1970 ◽  
Vol 48 (4) ◽  
pp. 418-424 ◽  
Author(s):  
D. J. Koerker ◽  
I. B. Fritz
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Respiratory Control ◽  
Liver Mitochondria ◽  
Acid Oxidation ◽  
Chick Embryos ◽  
Stage Of Development ◽  
Liver Slices ◽  
Hepatic Fatty Acid Oxidation ◽  
Carnitine Palmitoyltransferase Activity

The characteristics and developmental pattern of the metabolic pathway for fatty acid oxidation were investigated in liver slices and mitochondria prepared from chick embryos of varying ages. In 8-day-old chick embryos, hepatic fatty acid oxidation was readily measurable. The incorporation of labelled palmitate into CO2 was increased twofold by carnitine in liver slices of 8-day-old chick embryos but by nearly sixfold to tenfold in tissues prepared from 10- or 12-day-old embryos. A similar increase was seen in the degree of augmentation of ketogenesis induced by carnitine in liver slices prepared from the 10-day-old embryo, suggesting an increased carnitine palmitoyltransferase activity in liver cells during the stage of development from 8 to 10 days. Palmitoyl-CoA was not metabolized in the absence of carnitine, whereas the palmitoyl portion of palmitoylcarnitine readily supported respiration by embryonic chick liver mitochondria. In the presence of adequate amounts of albumin, good respiratory control was evident.The administration of glucose to chick eggs which had previously been incubated for approximately 4.5 days resulted in changes in the metabolism of embryos killed 5 days later, which indicated that tissues of the chick embryo were capable of integrative metabolic adaptations in response to changes in substrate supply.

scholarly journals Schistosoma mansoni does not and cannot oxidize fatty acids, but these are used for biosynthetic purposes instead

2018 ◽  
Author(s):  
Michiel L. Bexkens ◽  
Mirjam M. Mebius ◽  
Martin Houweling ◽  
Jos F. Brouwers ◽  
Aloysius G.M. Tielens ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Schistosoma Mansoni ◽  
Fatty Acid Oxidation ◽  
Egg Production ◽  
Neutral Lipids ◽  
Female Worm ◽  
Acid Oxidation ◽  
Genes Encoding

AbstractAdult schistosomes, parasitic flatworms that cause the tropical disease schistosomiasis, have always been considered to be homolactic fermenters and in their energy metabolism strictly dependent on carbohydrates. However, more recent studies suggested that fatty acid β-oxidation is essential for egg production by adult female Schistosoma mansoni. To address this conundrum, we performed a comprehensive study on the lipid metabolism of S. mansoni. Incubations with [14C]-labelled fatty acids demonstrated that adults, eggs and miracidia of S. mansoni did not oxidize fatty acids, as no 14CO2 production could be detected. We then re-examined the S. mansoni genome using the genes known to be involved in fatty acid oxidation in six eukaryotic model reference species. This showed that the earlier automatically annotated genes for fatty acid oxidation were in fact incorrectly annotated. In a further analysis we could not detect any genes encoding β-oxidation enzymes, which demonstrates that S. mansoni cannot use this pathway in any of its lifecycle stages. The same was true for S. japonicum. Absence of β-oxidation, however, does not imply that fatty acids from the host are not metabolized by schistosomes. Adult schistosomes can use and modify fatty acids from their host for biosynthetic purposes and incorporate them in phospholipids and neutral lipids. Female worms deposit large amounts of these lipids in the eggs they produce, which explains why interference with the lipid metabolism in females will disturb egg formation, even though fatty acid β-oxidation does not occur in schistosomes. Our analyses of S. mansoni further revealed that during the development and maturation of the miracidium inside the egg, changes in lipid composition occur which indicates that fatty acids deposited in the egg by the female worm are used for phospholipid biosynthesis required for membrane formation in the developing miracidium.

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