The effects of dietary fat on fatty acid synthesis and malic enzyme activity in liver from growing chicks

1969 ◽  
Vol 47 (7) ◽  
pp. 743-746 ◽  
Author(s):  
Alan G. Goodridge

Hepatic malic enzyme activity and incorporation of glucose-U-14C into fatty acids in liver slices was no greater in birds fed fat-free diets than in those fed the same diets supplemented with corn oil. The results suggest that in the chick, in contrast to the rat, dietary fat does not suppress hepatic lipogenesis.

1991 ◽  
Vol 69 (11) ◽  
pp. 1637-1647 ◽  
Author(s):  
Gene R. Herzberg

The level of circulating triacylglycerols is determined by the balance between their delivery into the plasma and their removal from it. Plasma triacylglycerols are derived either from dietary fat as chylomicrons or from endogenous hepatic synthesis as very low density lipoproteins. Their removal occurs through the action of lipoprotein lipase after which the fatty acids are either stored in adipose tissue or oxidized, primarily in skeletal muscle and heart. The composition of the diet has been shown to influence many of these processes. Hepatic fatty acid synthesis and triacylglycerol secretion are affected by the quantity and composition of dietary fat, carbohydrate, and protein. Polyunsaturated but not saturated fats reduce hepatic fatty acid synthesis by decreasing the amount of the lipogenic enzymes needed for de novo fatty acid synthesis. Dietary fish oils are particularly effective at reducing both fatty acid synthesis and triacylglycerol secretion and as a result are hypotriacylglycerolemic, particularly in hypertriacylglycerolemic individuals. In addition, dietary fish oils can increase the oxidation of fatty acids and lead to increased activity of lipoprotein lipase in skeletal muscle and heart. It appears that the hypotriacylglycerolemic effect of dietary fish oils is mediated by effects on both synthesis and removal of circulating triacylglycerols.Key words: lipid, fish oil, fructose, liver, adipose tissue, oxidation.


1980 ◽  
Vol 43 (3) ◽  
pp. 571-579 ◽  
Author(s):  
G. R. Herzberg ◽  
N. Janmohamed

The effect of varying dietary levels of maize oil and tripalmitin (0–250 g fat/kg) on hepatic lipogenesis and the levels of hepatic fatty acid synthetase (FAS), glucose-6-phosphate dehydrogenase (EC 1.1.1.49; G6PD), malic enzyme (EC 1.1.1.38, 1.1.1.39, 1.1.1.40; ME) and glucokinase (EC 2.7.1.2; GK) was examined in meal-fed mice.2. Meal-fed mice compared to mice fed ad lib. show enhanced hepatic lipogenesis as demonstrated by an increased rate of in vivo fatty acid synthesis and increased levels of FAS, ME and G6PD. The level of GK in meal-fed mice was unchanged by meal feeding.3. Maize oil more effectively reduced in vivo hepatic lipogenesis than tripalmitin in meal-fed mice.4. Maize oil more effectively reduced the hepatic levels of FAS, G6PD, ME and GK than tripalmitin in meal-fed mice.5. The increased inhibition by maize oil is observed at all levels of fat in the diet investigated and has been shown not to be due to decreased carbohydrate intake nor to differences between the absorption of maize oil and tripalmitin.


1968 ◽  
Vol 108 (4) ◽  
pp. 667-673 ◽  
Author(s):  
Alan G. Goodridge

1. The conversion of [U−14C]glucose into carbon dioxide, cholesterol and fatty acids in liver slices and the activities of ‘malic’ enzyme, citrate-cleavage enzyme, NADP-linked isocitrate dehydrogenase and hexose monophosphate-shunt dehydrogenases in the soluble fraction of homogenates of liver were measured in chicks that were starved or starved then fed. 2. In newly hatched chicks the incorporation of [U−14C]glucose and the activity of ‘malic’ enzyme did not increase unless the birds were fed. The response to feeding of [U−14C]glucose incorporation into fatty acids increased as the starved chicks grew older. 3. Citrate-cleavage enzyme activity increased slowly even when the newly hatched chicks were unfed. On feeding, citrate-cleavage enzyme activity increased at a much faster rate. 4. In normally fed 20-day-old chicks starvation decreased the incorporation of [U−14C]glucose into all three end products and depressed the activities of ‘malic’ enzyme and citrate-cleavage enzyme. Re-feeding increased all of these processes to normal or higher-than-normal levels. 5. In both newly hatched and 20-day-old chicks starvation increased the activity of isocitrate dehydrogenase and feeding or re-feeding decreased it. 6. Very little change in hexose monophosphate-shunt dehydrogenase activity was observed during the dietary manipulations. 7. The results indicate that increased substrate delivery to the liver is the principal stimulus to the increased rate of glucose metabolism observed in newly hatched chicks. The results also suggest that changes in the activities of ‘malic’ enzyme and citrate-cleavage enzyme are secondary to an increased flow of metabolites through the glucose-to-fatty acid pathway and that the dehydrogenases of the hexose monophosphate shunt play a minor role in NADPH production for fatty acid synthesis.


1969 ◽  
Vol 115 (4) ◽  
pp. 807-815 ◽  
Author(s):  
Stuart Smith ◽  
Harriet T. Gagné ◽  
Dorothy R. Pitelka ◽  
S. Abraham

1. Virgin and lactating C3H mice maintained on laboratory chow were transferred to a high-fat (15% corn oil) or a fat-free diet 3 days before being killed. 2. The linoleate content of liver, mammary gland and milk was decreased in lactating mice given the fat-free diet but was increased in those fed on the high-fat diet. Changes in linoleate content and mammary gland followed a similar but much less marked trend in virgin animals. 3. Hepatic fatty acid synthesis in lactating and virgin mice fed on the fat-free diet was higher than in corresponding animals fed on either the chow or the high-fat diet. The lipogenic capacity of livers from mice fed on either the chow or the high-fat diet was greater in lactating than in virgin animals. These changes in hepatic lipogenic capacity were accompanied by alterations in the specific activities of certain enzymes involved in fat synthesis. 4. Mammary gland from virgin and lactating animals showed no such adaptation to dietary fat. Results indicate that fatty acid synthesis in neither mammary-gland parenchymal cells nor mammary-gland adipose cells can be influenced by dietary fat in the same way as in the hepatocyte.


1967 ◽  
Vol 102 (3) ◽  
pp. 864-869 ◽  
Author(s):  
G. R. Jansen ◽  
M.E. Zanetti ◽  
C. F. Hutchison

1. The importance of fatty acid synthesis as a pathway for the disposal of ingested glucose has been evaluated in rats and mice given a purified diet high in glucose and low in fat. [U-(14)C]Glucose was either added to the diet and fed for 24hr. or given by stomach tube as a 250mg. (mice) or 1000mg. (rats) meal. The two methods of isotope administration gave similar results. 2. Under the conditions employed fatty acid synthesis appeared to be a more important pathway for glucose disposal in mice than in rats. In mice 15.3% of ingested [U-(14)C]glucose was converted into fatty acid and in rats the corresponding value was 8.6%. In contrast, the conversion of [U-(14)C]glucose into cholesterol, as a percentage of dose, was twice as high in rats as in mice. 3. The effect of 20% of corn oil in the diet on the conversion of dietary [U-(14)C]glucose into fat was also investigated. Mice given diets containing 1% or 20% of corn oil converted 14.6% or 7.0% respectively of dietary [U-(14)C]glucose into fatty acid over a 24hr. period. There was no effect of fat on the incorporation of the isotope into cholesterol. 4. In mice given diets containing 1% or 20% of corn oil approx. 10% and 2% respectively of newly synthesized fatty acids were found in the liver. Hepatic fatty acid synthesis appears to be more sensitive to dietary fat than is extrahepatic synthesis.


1972 ◽  
Vol 128 (5) ◽  
pp. 1057-1067 ◽  
Author(s):  
E. D Saggerson

1. 0.5mm-Palmitate stimulated incorporation of [U-14C]glucose into glyceride glycerol and fatty acids in normal fat cells in a manner dependent upon the glucose concentration. 2. In the presence of insulin the incorporation of 5mm-glucose into glyceride fatty acids was increased by concentrations of palmitate, adrenaline and 6-N-2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate up to 0.5mm, 0.5μm and 0.5mm respectively. Higher concentrations of these agents produced progressive decreases in the rate of glucose incorporation into fatty acids. 3. The effects of palmitate and lipolytic agents upon the measured parameters of glucose utilization were similar, suggesting that the effects of lipolytic agents are mediated through increased concentrations of free fatty acids. 4. In fat cells from 24h-starved rats, maximal stimulation of glucose incorporation into fatty acids was achieved with 0.25mm-palmitate. Higher concentrations of palmitate were inhibitory. In fat cells from 72h-starved rats, palmitate only stimulated glucose incorporation into fatty acids at high concentrations of palmitate (1mm and above). 5. The ability of fat cells to incorporate glucose into glyceride glycerol in the presence of palmitate decreased with increasing periods of starvation. 6. It is suggested that low concentrations of free fatty acids stimulate fatty acid synthesis from glucose by increasing the utilization of ATP and cytoplasmic NADH for esterification of these free fatty acids. When esterification of free fatty acids does not keep pace with their provision, inhibition of fatty acid synthesis occurs. Provision of free fatty acids far in excess of the esterification capacity of the cells leads to uncoupling of oxidative phosphorylation and a secondary stimulation of fatty acid synthesis from glucose.


1974 ◽  
Vol 142 (3) ◽  
pp. 611-618 ◽  
Author(s):  
D. Michael W. Salmon ◽  
Neil L. Bowen ◽  
Douglas A. Hems

1. Fatty acid synthesis de novo was measured in the perfused liver of fed mice. 2. The total rate, measured by the incorporation into fatty acid of3H from3H2O (1–7μmol of fatty acid/h per g of fresh liver), resembled the rate found in the liver of intact mice. 3. Perfusions with l-[U-14C]lactic acid and [U-14C]glucose showed that circulating glucose at concentrations less than about 17mm was not a major carbon source for newly synthesized fatty acid, whereas lactate (10mm) markedly stimulated fatty acid synthesis, and contributed extensive carbon to lipogenesis. 4. The identification of 50% of the carbon converted into newly synthesized fatty acid lends further credibility to the use of3H2O to measure hepatic fatty acid synthesis. 5. The total rate of fatty acid synthesis, and the contribution of glucose carbon to lipogenesis, were directly proportional to the initial hepatic glycogen concentration. 6. The proportion of total newly synthesized lipid that was released into the perfusion medium was 12–16%. 7. The major products of lipogenesis were saturated fatty acids in triglyceride and phospholipid. 8. The rate of cholesterol synthesis, also measured with3H2O, expressed as acetyl residues consumed, was about one-fourth of the basal rate of fatty acid synthesis. 9. These results are discussed in terms of the carbon sources of hepatic newly synthesized fatty acids, and the effect of glucose, glycogen and lactate in stimulating lipogenesis, independently of their role as precursors.


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