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In the present study the effects of some C18 fatty acids on hepatic fatty acid metabolism have been compared. Male rats were fed cholesterol-free diets containing either C18:0, C18:1cis or C18:1trans isomers as the variables. In accordance with previous work, oleic acid in the diet caused an increase in cholesterol concentration in the liver and in the lipoprotein fraction of density (d; kg/l)<1·006. Oleic acid also reduced the triacylglycerol:cholesterol value in this fraction. Surprisingly, the C18:1trans isomers diet induced a decrease in the amount of cholesterol in total plasma as well as in the 1·019<d<1·063 lipoprotein fraction. Both oleic acid and C18:1trans isomers increased the concentration of triacylglycerols in the liver. The two C18:1 fatty acids differently influenced the hepatic activities of carnitine palmitoyltransferase-I and 3-hydroxy-acyl-CoA dehydrogenase; both enzymes were inhibited by C18:1trans isomers, while no change was induced by oleic acid. The activity of the citrate carrier was lower in the oleic acid- and C18:1trans isomers-fed rats, when compared with the rats fed stearic acid. No diet effects were seen for the activities of acetyl-CoA carboxylase, fatty acid synthase, diacylglycerol acyltransferase, citrate synthase and phosphofructokinase. The results are interpreted in that oleic acid raised liver triacylglycerol by reducing the secretion of it with the d<1·006 lipoprotein fraction whereas the C18:1trans isomers enhanced liver triacylglycerol by lowering the hepatic oxidation of fatty acids.
The metabolic effects of feeding soyabean oil instead of an isoenergetic amount of maize starch plus glucose were studied in ponies. Twelve adult Shetland ponies were given a control diet (15 g fat/kg DM) or a high-fat diet (118 g fat/kg DM) according to a parallel design. The diets were fed for 45 d. Plasma triacylglycerol (TAG) concentrations decreased by 55 % following fat supplementation. Fat feeding also reduced glycogen concentrations significantly by up to 65 % in masseter, gluteus and semitendinosus muscles (P<0·05, P<0·01 and P<0·01 respectively). The high-fat diet significantly increased the TAG content of semitendinosus muscle by 80 % (P<0·05). Hepatic acetyl-CoA carboxylase and fatty acid synthase activities were 53 % (P<0·01) and 56 % (P<0·01) lower respectively in the high-fat group, but diacylglycerol acyltransferase activity was unaffected. Although carnitine palmitoyltransferase-I (CPT-I) activity in liver mitochondria was not influenced, fat supplementation did render CPT-I less sensitive to inhibition by malonyl-CoA. There was no significant effect of diet on the activity of phosphofructokinase in the different muscles. The activity of citrate synthase was raised significantly (by 25 %; P<0·05) in the masseter muscle of fat-fed ponies, as was CPT-I activity (by 46 %; P<0·01). We conclude that fat feeding enhances both the transport of fatty acids through the mitochondrial inner membrane and the oxidative capacity of highly-aerobic muscles. The higher oxidative ability together with the depressed rate of de novo fatty acid synthesis in liver may contribute to the dietary fat-induced decrease in plasma TAG concentrations in equines.
The hypothesis that olive-oil consumption alters plasma sphingomyelin concentrations and hepatic sphingomyelin metabolism was tested. Rats were fed on purified, high-cholesterol diets with either coconut fat or olive-oil (180 g/kg). In accordance with previous work, olive-oil v. coconut-fat consumption significantly elevated hepatic and total plasma cholesterol concentrations. During the course of the experiment, the concentration of plasma sphingomyelin rose in the coconut-fat group and remained constant in the olive-oil group. When compared with the coconut-fat-fed group, the plasma sphingomyelin levels were significantly lower in the olive-oil-fed group after 14 and 21 d of treatment. Dietary olive oil raised the amounts of cholesterol and sphingomyelin in the VLDL density region, and this change was associated with a reduction in the cholesterol and sphingomyelin contents of the LDL and HDL density ranges. Olive-oil consumption reduced the activity of serine palmitoyltransferase, while the activities of phosphatidylcholine:ceramide cholinephosphotransferase and phosphatidylethanolamine:ceramide ethanolaminephosphotransferase were left unchanged. Dietary olive oil also enhanced the activity of acidic sphingomyelinase, but not that of neutral sphingomyelinase. The present data indicate that dietary olive oil v. coconut fat has opposite effects on total plasma cholesterol and sphingomyelin concentrations. The lower plasma sphingomyelin levels observed in olive-oil-fed, as compared with coconut-fat-fed rats, may be explained by a simultaneous elevation and reduction in sphingomyelin catabolism and synthesis respectively, as based on the measured enzyme activities.
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