Differential effects of dietary methyl esters of long-chain saturated and polyunsaturated fatty acids on rat liver and adipose tissue lipogenesis (original) (raw)
Related papers
The Journal of Nutrition, 1977
Rats were trained to eat a fat-free high carbohydrate diet from 800 to 1100 hours each day. After adaptation to meal-eating, the fatfree diet was supplemented with 8% methyl stéarate(Ci8;o) or 3% methyl linoleate (Ci8:2) for 7 days. Relative to the fat-free group, hepatic utiliza tion of acetate unit equivalents (C2 units) for fatty acid synthesis per mg soluble protein by the Ci8:o group was not significantly altered, whereas Ci8:2 supplementation significantly depressed hepatic fatty acid synthesis. Supplemental Ci8:2 also caused a significant decline in liver fatty acid synthetase and acetyl CoA carboxylase while fat-free and Ci8:o groups dis played similar enzyme activities. Within a treatment, C2 unit utilization tor in vivo fatty acid synthesis was identical to that of acetyl CoA car boxylase and fatty acid synthetase activities in vitro. Therefore, shortly after a meal, the hepatic activities of these two enzymes appear to be functioning at near capacity. Ci8:2 supplementation to the fat-free diet for 7 days caused a 25% decline in glucokinase and pyruvate kinase activ ities, but only pyruvate kinase was significantly depressed. In contrast, citrate cleavage enzyme and fatty acid synthetase were both significantly reduced in activity by 50%. Plasma unesterified fatty acid levels in rats fed Ci8:2 for 5 days were not significantly elevated prior to a meal, al though dietary Ci8:2 did cause a fourfold rise in plasma free linoleate. Quantitation of long chain acyl CoA esters in freeze-clamped liver tissue of rats fed fat-free or fat-free plus 3% Ci8:2 or Ci8:3 diets revealed no con centration differences between treatments either before or after a meal. Similarly, lactate and pyruvate concentrations as well as the lactate: pyru vate ratios were not significantly changed by dietary Ci8:2 or Ci8:3. The inhibitory effects of C18:2 or Ci8;3 appear not to be mediated through changes in total plasma free fatty acid levels, in total hepatic long chain acyl CoA concentration or in hepatic cytosolic redox state.
2010
Rats were trained to eat a fat-free high carbohydrate diet from 800 to 1100 hours each day. After adaptation to meal-eating, the fatfree diet was supplemented with 8% methyl stéarate(Ci8;o) or 3% methyl linoleate (Ci8:2) for 7 days. Relative to the fat-free group, hepatic utiliza tion of acetate unit equivalents (C2 units) for fatty acid synthesis per mg soluble protein by the Ci8:o group was not significantly altered, whereas Ci8:2 supplementation significantly depressed hepatic fatty acid synthesis. Supplemental Ci8:2 also caused a significant decline in liver fatty acid synthetase and acetyl CoA carboxylase while fat-free and Ci8:o groups dis played similar enzyme activities. Within a treatment, C2 unit utilization tor in vivo fatty acid synthesis was identical to that of acetyl CoA car boxylase and fatty acid synthetase activities in vitro. Therefore, shortly after a meal, the hepatic activities of these two enzymes appear to be functioning at near capacity. Ci8:2 supplementation to the fat-free diet for 7 days caused a 25% decline in glucokinase and pyruvate kinase activ ities, but only pyruvate kinase was significantly depressed. In contrast, citrate cleavage enzyme and fatty acid synthetase were both significantly reduced in activity by 50%. Plasma unesterified fatty acid levels in rats fed Ci8:2 for 5 days were not significantly elevated prior to a meal, al though dietary Ci8:2 did cause a fourfold rise in plasma free linoleate. Quantitation of long chain acyl CoA esters in freeze-clamped liver tissue of rats fed fat-free or fat-free plus 3% Ci8:2 or Ci8:3 diets revealed no con centration differences between treatments either before or after a meal. Similarly, lactate and pyruvate concentrations as well as the lactate: pyru vate ratios were not significantly changed by dietary Ci8:2 or Ci8:3. The inhibitory effects of C18:2 or Ci8;3 appear not to be mediated through changes in total plasma free fatty acid levels, in total hepatic long chain acyl CoA concentration or in hepatic cytosolic redox state.
2010
Rats were meal-fed once daily methyl esters of palmitate (Ci6:o); stéarate(Ci8:0); linoleate (C18:2) and linolenate (Ci8:3) to de termine the influence of these fatty acids on glucokinase and fatty acid synthetase activities and on in vivo rates of fatty acid synthesis in the liver. Addition of 1% Ci6:0 or 3% C18:3to a fat-free basal diet did not alter the rate at which the diet was removed from the stomach and small intestine. Consumption of a diet containing Ci8:2 for eight meals significantly re duced hepatic fatty acid synthetase activity and in vivo rates of fatty acid synthesis by 40%, but did not alter glucokinase activity. At least three meals of a diet containing C18:2or Ci8:3 were required to inhibit hepatic fatty acid synthesis. Conversely, after rats consumed Ci8:2, more than two meals of a fat-free diet were required to increase hepatic rates of fatty acid synthesis. Dietary C18:oand C18:0did not alter rates of fatty acid synthesis in rat liver. Glucokinase was not inf...
Biochimica Et Biophysica Acta (bba) - Lipids and Lipid Metabolism, 1982
When mice, previously fed a standard laboratory mouse chow diet, were fed a high carbohydrate (50% glucose) diet containing 15% (w/w) hydrogenated cottonseed oil, the activity of hepatic fatty acid synthetase per mg cytosolic protein increased approximately 3-fold over an 11-day period. However, when mice were placed on an isocaloric diet containing 15% (w/w) corn oil, the specific activity of the enzyme did not increase above the chow-fed levels. Using antibody prepared against pure mouse liver fatty acid synthetase, we showed that the increase in the specific activity of fatty acid synthetase in the hydrogenated cottonseed oil-fed animals resulted from an elevation in the hepatic content of the enzyme. This increase was a result of (a) an increase in the rate of synthesis of the enzyme relative to that of total protein and (b) a decrease in the enzyme's degradative rate, when compared to these parameters measured in the livers of the corn oil-fed animals. Furthermore, these dietary-induced changes in enzyme specific activity were not a~ompanied by changes in the catalytic efficiency of fatty acid synthetase; since both hydr~nat~ cottonseed oil-fed and corn oil-fed animals showed identical immn~oequivalences and contained similar amounts of immunoprecip itable 3H-labeled enzyme protein per unit enzyme activity (in mice pulse-labeled with [3H]leucine). The results of experiments in which we administered pure fatty acids (oleic (cis -A9sp-18: l), ricinoleic (12-hydroxycis-A9-18: l), linoleic (cis* &-A 9%12-18:2), cw-linoleic (cis, ck &A 9,'2~15 -18: 3), columbinic (kurs, cis, c&A-5,9,'2-18:3) and arachidonic (all-&-d s,s,r'*f4-20:4)) to mice maintained on a 50% glucose diet suggested that the ability of a fatty acid to inhibit hepatic fatty acid synthetase activity and to prevent an increase in hepatic fatty acid synthetase protein was related to the degree and position of unsaturation of the fatty acid administered and not to the ability of the fatty acid to act as prostaglandin precursor. Those 9~12 IS-carbon fatty acids which possessed a double bond at positions A (linoleic, eolumbinic and o-linolenic) were the most effective at inhibiting hepatic fatty acid synthetase activity and in preventing an increase in enzyme content.
Journal of Nutrition
Rats were meal-fed once daily methyl esters of palmitate (Ci6:o); stéarate(Ci8:0); linoleate (C18:2) and linolenate (Ci8:3) to de termine the influence of these fatty acids on glucokinase and fatty acid synthetase activities and on in vivo rates of fatty acid synthesis in the liver. Addition of 1% Ci6:0 or 3% C18:3to a fat-free basal diet did not alter the rate at which the diet was removed from the stomach and small intestine. Consumption of a diet containing Ci8:2 for eight meals significantly re duced hepatic fatty acid synthetase activity and in vivo rates of fatty acid synthesis by 40%, but did not alter glucokinase activity. At least three meals of a diet containing C18:2 or Ci8:3 were required to inhibit hepatic fatty acid synthesis. Conversely, after rats consumed Ci8:2, more than two meals of a fat-free diet were required to increase hepatic rates of fatty acid synthesis. Dietary C18:o and C18:0did not alter rates of fatty acid synthesis in rat liver. Glucokinase was not influenced by any of the methyl esters fed in all trials except one. The results of this study suggest that polyunsaturated fatty acids can specifically influence hepatic fatty acid syn thesis and fatty acid synthetase activity without altering glucokinase activity, and that meal-fed rats must consume at least three meals con taining polyunsaturated fatty acids before hepatic fatty acid synthesis or fatty acid synthetase activity is altered.
Hepatic fatty acid metabolism in rats fed diets with different
2003
In the present study the effects of some C 18 fatty acids on hepatic fatty acid metabolism have been compared. Male rats were fed cholesterol-free diets containing either C 18 : 0 , C 18 : 1 cis or C 18 : 1 trans 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 C 18 : 1 trans 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 C 18 : 1 trans isomers increased the concentration of triacylglycerols in the liver. The two C 18 : 1 fatty acids differently influenced the hepatic activities of carnitine palmitoyltransferase-I and 3-hydroxy-acyl-CoA dehydrogenase; both enzymes were inhibited by C 18 : 1 trans isomers, while no change was induced by oleic acid. The activity of the citrate carrier was lower in the oleic acid-and C 18 : 1 trans 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 C 18 : 1 trans isomers enhanced liver triacylglycerol by lowering the hepatic oxidation of fatty acids.
British Journal of Nutrition, 1995
Thirty male rats were randomly assigned to one of three dietary groups in which the source of dietary fat was either a mixed oil, maize oil or fish oil. Effects of dietary fatty acid composition onin vitrorates of [U-14C]glucose incorporation into hepatic total lipids and into hepatic triacylglycerol were measured under basal, insulin (4 nM)-, gastric inhibitory polypeptide (GIP; 6 nM)- and insulin + GIP (4 nM + 6nM)-stimulated conditions. Effects of the three diets on postprandial plasma triacylglycerol, cholesterol, insulin and GIP concentrations were also measured. The fish-oil diet decreased rates of basal glucose incorporation into hepatic total lipids (P< 0·05) and hepatic triacylglycerol (P< 0·01) compared with the mixed-oil diet. The presence of insulin and GIP in the incubation medium stimulated glucose incorporation into hepatic total lipids in the maize-oil (P< 0·01) and fish-oil groups (P< 0·05), as well as into hepatic triacylglycerol in the maize-oil group ...
British Journal of Nutrition, 2003
In the present study the effects of some C 18 fatty acids on hepatic fatty acid metabolism have been compared. Male rats were fed cholesterol-free diets containing either C 18 : 0 , C 18 : 1 cis or C 18 : 1 trans 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 C 18 : 1 trans 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 C 18 : 1 trans isomers increased the concentration of triacylglycerols in the liver. The two C 18 : 1 fatty acids differently influenced the hepatic activities of carnitine palmitoyltransferase-I and 3-hydroxy-acyl-CoA dehydrogenase; both enzymes were inhibited by C 18 : 1 trans isomers, while no change was induced by oleic acid. The activity of the citrate carrier was lower in the oleic acid-and C 18 : 1 trans 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 C 18 : 1 trans isomers enhanced liver triacylglycerol by lowering the hepatic oxidation of fatty acids.