Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.4.1.2 (acetyl-CoA carboxylase)
 2,876 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipogenesis has been investigated in diploid fibroblasts derived from patients with familial hypertriglyceridaemia (FHT) and compared with cells from healthy persons. There was no difference in acetyl-CoA carboxylase activity in both cell types. Incorporation of [2-14C]-acetate into triglyceride fatty acids was slightly increased (34%) by the FHT lines. Addition of triiodothyronine caused a marked rise in [2-14C]-acetate incorporation by the FHT lines whereas the normal lines exhibited only control values. Maximal rise in [2-14C]-acetate incorporation was obtained with 5 micrograms/ml for 72 h. Under these conditions, acetate incorporation by the FHT lines was 220% of the controls, compared with 94% by the normal lines. Measurements of acetyl-CoA carboxylase specific activity supported the results obtained with measurements of acetate incorporation into triglyceride fatty acids. Individual FHT lines differ much in their quantitative answer to thyroid hormones, although the described effects were obtained with all eight lines under study. Insulin increased acetyl-CoA carboxylase activity and incorporation of [2-14C]-acetate in lipids in both cell types, but with no difference between normal and FHT lines. The results seem to reflect a higher lipogenic capacity of the hypertriglyceridaemic fibroblasts compared with normal cells.
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PMID:Hormonal regulation of lipogenesis in human diploid fibroblasts from normal subjects and from patients with familial hypertriglyceridaemia. 613 14

The extent of fatty acid synthesis from [1-14C]acetate in liver slices was reduced 6-fold when eels were fasted for 1-7 weeks and 20-fold when fasted for 39 weeks; thereafter hepatic lipogenesis seemed to remain constant for up to 95 weeks of fasting. After a 1-3 week fast some hepatic enzyme activities were reduced (acetyl-CoA carboxylase decreased 2-fold and fatty acid synthetase declined 5-fold), while others remained unchanged (glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, alpha-glycerol phosphate dehydrogenase as well as malic enzyme and ATP-citrate lyase). The optimum temperature for measuring both total lipid synthesis and lipogenic enzyme activity in eel liver was found to be 30 degrees C.
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PMID:The effect of prolonged fasting on total lipid synthesis and enzyme activities in the liver of the European eel (Anguilla anguilla). 615 Aug 5

Octanoate and N6,O2'-dibutyryl adenosine 3',5'-monophosphate (dibutyryl cyclic AMP) cause a marked inhibition of net glucose utilization and lactate and pyruvate accumulation by hepatocytes isolated from meal-fed rats. Acetate is much less effective as an inhibitor of glycolysis. Fatty acid synthesis, as measured by tritiated water incorporation, is inhibited by dibutyryl cyclic AMP, whereas it is stimulated by 10 mM acetate and 1 mM octanoate. Stimulation of fatty acid synthesis by 1 mM octanoate, however, is lost paradoxically at higher concentrations of octanoate. Rates of fatty acid synthesis estimated by [1-14C]octanoate incorporation were consistently higher than rates calculated on the basis of tritiated water incorporation, raising the question as to which is the better index of the rate of de novo fatty acid synthesis. The effects of octanoate were studied because it was reasoned that this fatty acid should not inhibit acetyl-CoA carboxylase but should inhibit glycolysis and supply acetyl-CoA for lipogenesis. This was found to be the case, proving that glycolytic activity is not necessary for rapid rates of de novo fatty acid synthesis by liver.
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PMID:Effects of octanoate and acetate upon hepatic glycolysis and lipogenesis. 631 44

Studies of lipid metabolism in cell cultures are usually carried out after preincubation of cells in media containing lipoprotein-deficient or delipidated serum. The artifacts produced during delipidation prevent the standardization of assays and the study of the role of hormones on lipid metabolism. We studied the effects of triiodothyronine, hydrocortisone, insulin and their combination on cholesterol and fatty acid synthesis in cultured human skin fibroblasts preincubated for 24 h in an artificial medium (medium A) consisting of equal volumes of Dulbecco's modified Eagle's and Ham's F-12 media enriched with transferrin, biotin and calcium pantothenate. In cells preincubated in medium A the incorporation of acetate to cholesterol and the activity of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase were much lower than in cells preincubated in standard medium containing lipoprotein-deficient serum. Addition of the three hormones caused a marked stimulation of the incorporation of acetate to cholesterol (from 3.1 to 17.7 pmol/min per mg protein), an activity similar to that in cells preincubated in lipoprotein-deficient serum plus hormones. The stimulatory effect of the hormones on HMG-CoA reductase activity was smaller, from 11 to 26 pmol/min per mg protein compared to 83 pmol/min per mg protein in cells preincubated in lipoprotein-deficient serum plus hormones. Most of the stimulatory effect was due to insulin. The lack of coordinate response between these two parameters in cells preincubated in artificial medium could not be explained by (a) stimulation of a post-mevalonate step as measured by the incorporation of mevalonate to cholesterol; (b) the in vitro inactivation of HMG-CoA reductase by phosphorylation: incubation of fibroblast microsomes with Escherichia coli alkaline phosphatase resulted in a decrease in HMG-CoA reductase activity, in contrast to an increase in hepatic microsomes; (c) the presence of inhibitors of HMG-CoA reductase in the microsomal extract. In cells preincubated in medium A the incorporation of acetate to fatty acids and the activities of acetyl-CoA carboxylase and fatty acid synthetase were approximately equal to that of cells preincubated in standard medium containing lipoprotein-deficient serum. Hormones added to medium A caused a stimulation of incorporation of acetate to fatty acids (from 5.1 to 19.8 pmol/min per mg protein), the activity of acetyl-CoA carboxylase (from 494 to 820 pmol/min per mg protein) and of fatty acid synthetase (from 300 to 678 pmol/mg protein). These values were significantly higher than those obtained in cells preincubated with lipoprotein-deficient serum with or without hormones.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effects of triiodothyronine, hydrocortisone and insulin on lipid synthesis by cultured fibroblasts preincubated in a serum-free medium. 636 71

The effect of hypolipidemic drugs, WY14643 and DH990, on plant lipid metabolism has been studied. The total incorporation of [14C]acetate into lipids was inhibited by addition of both drugs to aged potato (Solanum tuberosum) tuber discs, spinach (Spinacia oleracea) leaves, and spinach chloroplasts, while the incorporation in Chlorella vulgaris cells was affected only by DH990. Moreover, DH990 inhibited the incorporation of 14C-labeled fatty acids into phosphatidylcholine and phosphatidylethanolamine of potato discs, and decreased the incorporation into phosphatidylglycerol of Chlorella cells. DH990 inhibited the formation of polyunsaturated fatty acids in potato discs, Chlorella cells, and spinach leaves, whereas WY14643 had no effect on the formation of these fatty acids. Stearoyl-ACP desaturase from safflower (Carthamus tinctorius) seeds was very sensitive to both drugs, especially DH990, which completely blocked the activity at 2 mM levels. When safflower lysophospholipid acyltransferases were solubilized by detergent treatment, only DH990 inhibited the incorporation of [14C]oleoyl-CoA into lysophosphatidylcholine or lysophosphatidylethanolamine. Both drugs inhibited fatty acid synthesis from [14C]malonyl-CoA in the microsomal fraction from safflower seeds, but only DH990 inhibited FAS activity in the soluble fraction; both drugs inhibited severely the formation of stearic acid. Both acetyl-CoA carboxylase and acetyl-CoA synthetase were sensitive to both drugs.
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PMID:The effect of hypolipidemic drugs on plant lipid metabolism. 648 26

Subcutaneous adipose tissue samples were obtained by biopsy technique and at slaughter from steers fed either a corn concentrate or pelleted alfalfa (roughage) diet. Steers fed the roughage diet had slightly greater metabolizable energy intakes than the concentrate-fed steers due to greater rates of feed intake; however, steers fed the concentrate diet had faster rates of gain, primarily in the fat depots. Diet had no effect on the incorporation of 14C-labeled acetate and lactate into fatty acids, although 3H2O incorporation into fatty acids was greater in the concentrate-fed steers. Although backfat thickness was 60% greater in the concentrate-fed steers, the number of adipocytes per gram adipose tissue was unaffected by diet, suggesting adipose cell hyperplasia. The activities of acetyl-CoA carboxylase, fatty acid synthetase, ATP citrate lyase, NADP+ malate dehydrogenase, and hexokinase were greater in the steers fed the concentrate diet; pyruvate kinase activity was unaffected by diet. Fatty acid synthesis and several lipogenic enzyme activities increased with age and then declined markedly by the time of the terminal biopsy. Basal and net rates of lipolysis generally were unaffected by diet but increased with age of the animal. As the animals gained weight, the ratio of net fatty acids released to glycerol released decreased, suggesting more extensive reesterification of fatty acids released during lipolysis.
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PMID:Interrelationships among diet, age, fat deposition and lipid metabolism in growing steers. 669 76

The effects of tunicamycin on 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity and cholesterol biosynthesis have been studied in cultured C-6 glial cells. Depending on culture conditions, exposure to tunicamycin caused either a marked inhibition of induction of HMG-CoA reductase activity or, under steady state conditions, a marked reduction in enzymatic activity. Incorporation of [14 C]acetate into sterols was affected similarly. After a 24-h exposure, a 50% reduction in reductase activity was observed with a concentration of 0.05 micrograms/ml, and a maximal, 65-70% reduction occurred with 0.10 micrograms/ml of the drug. The effect of tunicamycin on reductase activity and on sterol synthesis was apparent 4 h after addition of the drug and nearly maximal after 6 h. The relative specificity of the effect of tunicamycin was indicated by the finding of no change in the activities of NADPH-cytochrome c reductase, acetyl-CoA carboxylase, or fatty acid synthetase, in incorporation of [3H]leucine into total protein, or in the rate of increase in cellular protein and phospholipid at concentrations of tunicamycin that caused the marked effect on HMG-CoA reductase. The reversibility of the effect of tunicamycin was shown by observing total recovery of reductase activity within 24 h after removal of the drug following a 24-h exposure. That the effect of tunicamycin on reductase is related to the drug's effect on glycoprotein synthesis was shown in two ways. First, the range of concentrations over which tunicamycin led to the decrease in reductase activity was essentially identical with the range over which the drug led to a decrease in incorporation of [3H]mannose into protein. Second, incubation of C-6 cells with N-acetylglucosamine simultaneously with tunicamycin was accompanied by prevention of the drug's effect on both HMG-CoA reductase and glycoprotein synthesis. These data suggest that glycoprotein synthesis is necessary for the expression of HMG-CoA reductase activity and, thereby, cholesterol synthesis in glial cells. Moreover, a link between glycoprotein and cholesterol biosynthesis could play a role in the mediation of certain maturational events in cells of neural origin.
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PMID:Effect of tunicamycin on 3-hydroxy-3-methylglutaryl coenzyme A reductase in C-6 glial cells. 687 86

1. The mean volume of adipocytes, the rates of fatty acid and acylglycerol glycerol synthesis from various precursors (in vitro), the rates of oxidation of acetate and glucose (in vitro) and the activities of lipoprotein lipase and various lipogenic enzymes were determined for perirenal adipose tissue from foetal lambs during the last month of gestation. 2. The fall in the rate of growth of perirenal adipose tissue during the last month of gestation is associated with a diminished capacity for fatty acid synthesis and lipoprotein lipase activity, but no change in the rate of acylglycerol glycerol synthesis was observed. There was no fall in the activities of cytosolic acetyl-CoA synthetase or the NADP-linked dehydrogenases, suggesting that the decrease in the rate of fatty acid synthesis was due to an impairment at the level of acetyl-CoA carboxylase or fatty acid synthetase. 3. The rate of fatty acid synthesis from acetate was greater than that from glucose. The rate of fatty acid synthesis from glucose per adipocyte of foetal lambs was similar to that of young sheep. The characteristic metabolism of adipose tissue of the adult sheep is thus present in the foetus, despite the relatively large amounts of glucose in the foetal 'diet'.
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PMID:Aspects of adipose-tissue metabolism in foetal lambs. 703 12

Rates of fatty acid synthesis from lactate and acetate and activities of selected lipogenic and NADPH-generating enzymes were determined in subcutaneous, intermuscular and intramuscular adipose tissues of cattle that were 11-19 months of age. Fatty acid synthesis from lactate and acetate increased from 11 to 13 months of age in subcutaneous and intermuscular adipose tissues; synthesis from lactate increased until 17 months of age. In intramuscular adipose tissue, synthesis from lactate also increased until 17 months of age while that from acetate continually increased. Activities of NADPH-generating enzymes increased in all three fat depots from 11 to 13 months of age, and little change occurred thereafter. Acetyl-CoA carboxylase activity was constant over entire growth period in all depots. Activity of ATP-citrate lyase increased from 11 to 13 months of age in subcutaneous and intermuscular adipose tissues, but did not increase until 19 months of age in intramuscular adipose tissue. In all cases, activities of ATP-citrate lyase were sufficient to support synthesis from lactate; therefore, lactate conversion to fatty acids in bovine adipose tissues seems to use the citrate cleavage pathway for generation of cytosolic acetyl-CoA.
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PMID:Fatty acid synthesis from lactate in growing cattle. 726 74

Crossbred steers (seven to nine per treatment) fed a pelleted alfalfa hay diet were biopsied (preinfusion) to obtain subcutaneous adipose tissue (SAT). Five days later a continuous intravenous infusion was begun of either 0.9% NaCl, glucose (2.75 moles/day), DL-lactate (5.5 moles/day of L-lactate), propionate (5.5 moles/day) or acetate (8.25 moles/day); after infusion for 14 days, a second biopsy sample of SAT was obtained. Glucose and DL-lactate infusion increased acetyl-CoA carboxylase activity about 12-fold compared to preinfusion activity of 5.3 +/- 4.2 nmoles/minute/g of wet weight. Glucose infusion induced activities of fatty acid synthetase (2.6 fold) and NADP+-malate dehydrogenase (7-fold) relative to preinfusion activities of 26.8 +/- 5.2 and 30.3 +/- 15.5 nmoles/minute/g of wet weight, respectively. Glucose, DL-lactate and propionate infusion increased NADP-isocitrate dehydrogenase activity 20-30% compared to preinfusion activity. Activity of NAD-malate dehydrogenase was not altered by any infusion treatment (P > 0.05). Activity of ATP-citrate lyase was decreased 48% by lactate infusion. Glucose, lactate and propionate infusion increased the rates of lactate and glucose incorporation into fatty acids in SAT incubated in vitro three to fourfold over preinfusion incorporation rates. Increased availability of glucose or gluconeogenic precursors may be responsible for induction of lipogenesis in steers fed high concentrate diets.
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PMID:Effects of intravenous infusions of glucose, lactate, propionate or acetate on the induction of lipogenesis in bovine adipose tissue. 742 Feb 5


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