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)

In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver, whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) ("coconut oil diet") or linseed oil (80 g/kg) ("linseed oil diet") as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Zinc deficiency and activities of lipogenic and glycolytic enzymes in liver of rats fed coconut oil or linseed oil. 776 Jun 90

We examined changes in the enzyme activities and metabolites related to hepatic fatty acid synthesis in fasted rats with sepsis produced by cecal ligation and puncture. Sepsis stimulated the in vivo incorporation of tritiated water into hepatic fatty acids and nonsaponifiable lipids. The activities of acetyl-CoA carboxylase, ATP-citrate lyase, and NADPH-generating enzymes (glucose-6-phosphate dehydrogenase and malic enzyme), the tissue levels of citrate and malonyl-CoA, and the dephosphorylation of carboxylase were increased in the livers of fasted septic rats compared with fasted sham-operated control rats. These results indicate that sepsis stimulated hepatic lipogenesis and sterologenesis in fasting rats. Furthermore, sepsis reduced the specific activity of hepatic mitochondrial carnitine palmitoyltransferase and raised that of glycerophosphate acyltransferase, suggesting an increased diversion of cytosolic acyl-CoA towards esterification. These intrahepatic metabolic changes strongly suggest that sepsis causes anabolic action on hepatic lipid metabolism.
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PMID:Accelerated hepatic lipid synthesis in fasted septic rats. 809 11

The time courses and the regulation of lipogenic enzyme gene expression during development after birth have been investigated. The mRNA concentrations and activities of liver lipogenic enzymes (acetyl-CoA carboxylase, fatty acid synthase, malic enzyme, glucose-6-phosphate dehydrogenase, and ATP-citrate lyase) were very low in all the suckling rats, regardless of dietary fat of the mothers. After weaning to the same diet as the mothers, the mRNA and enzyme levels were greatly increased by the fat-free or hydrogenated fat diet but not so greatly increased by the corn or fish oil diet. The mRNA concentrations of all the groups reached maximum at 4-6 weeks old and then decreased, usually to 40-60% of the maximal levels. It appeared that the gene expression after weaning is subject to strong nutritional regulation, as well as developmental regulation. The plasma levels of triiodothyronine and insulin were low during suckling. Malic enzyme mRNA level was increased by triiodothyronine treatment even during suckling, but the absolute increase was much less than after weaning. Thus, the gene expression of lipogenic enzymes during suckling appeared to be suppressed by nutritional and hormonal regulation, or may not be sufficiently developed. On the other hand, the hepatic triacylglycerol levels were increased slightly at 2 weeks old and greatly at 3 weeks. As the gene expression of lipogenic enzymes was still low at that time, the major triacylglycerols appear to be obtained from milk and accumulated in preparation for weaning.
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PMID:Lipogenic enzyme gene expression in rat liver during development after birth. 810 37

The effects of dietary phytosterols on lipid metabolism have been assessed through determination of liver lipids (sterols and fatty acids) and lipid metabolism enzymes (acetyl-CoA carboxylase, malic enzyme, glucose-6-phosphate dehydrogenase) in rats fed 12 or 24 mg cholesterol a day and 0-96 mg phytosterols. The results indicate that, provided the dietary phytosterol to cholesterol ratio is at least 1 and in the presence of a dietary cholesterol excess, phytosterols do exert a regulatory role through decreases of both acetyl-CoA carboxylase and malic enzyme activities. A ratio of 2 enhances this effect. At the same time, liver fatty acids and cholesterol contents significantly decrease.
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PMID:Effects of dietary phytosterols on liver lipids and lipid metabolism enzymes. 810 80

The effect of fibric acid derivatives, clofibric acid (CFB), bezafibrate (BFB), and gemfibrozil (GFB) on hepatic cytosolic enzymatic activities involved in saturated fatty acid synthesis has been estudied in vitro. From all the activities tested (fatty acid synthetase, acetyl-CoA carboxylase, ATP-citrate lyase, malic enzyme, malic dehydrogenase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase), only acetyl-CoA carboxylase and glucose-6-phosphate dehydrogenase were significantly inhibited by fibrates, with the following order of potency: GFB > BFB > > CFB. The characteristics of the inhibition phenomena (IC50, kinetic analysis, time and protein dependence, etc) and their transcendence to the effects of fibric acid derivatives in vivo are discussed.
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PMID:Cytosolic lipogenic enzymes: effect of fibric acid derivatives in vitro. 835 62

The effect of eicosapentaenoic acid (EPA) on fatty acid oxidation and on key enzymes of triglyceride metabolism and lipogenesis was investigated in the liver of rats. Repeated administration of EPA to normolipidemic rats resulted in a time-dependent decrease in plasma triglycerides, phospholipids and cholesterol. The triglyceride-lowering effect was observed after one day of feeding whereas lowering of plasma cholesterol and phospholipids was observed after five days of treatment. The triglyceride content of liver was reduced after two-day treatment. At that time, increased mitochondrial fatty acid oxidation occurred whereas mitochondrial and microsomal glycerophosphate acyltransferase was inhibited. The phosphatidate phosphohydrolase activity was unchanged. Adenosine triphosphate:citrate lyase, acetyl-CoA carboxylase, fatty acid synthetase and glucose-6-phosphate dehydrogenase were inhibited during the 15 d of EPA treatment whereas peroxisomal beta-oxidation was increased. At one day of feeding, however, when the hypotriglyceridemic effect was established, the lipogenic enzyme activities were reduced to the same extent in palmitic acid-treated animals as in EPA-treated rats. In cultured rat hepatocytes, the oxidation of [14C]palmitic acid to carbon dioxide and acid-soluble products was stimulated in the presence of EPA. These results suggest that the instant hypolipidemia in rats given EPA could be explained at least in part by a sudden increase in mitochondrial fatty acid oxidation, thereby reducing the availability of fatty acids for lipid synthesis in the liver for export, e.g., in the form of very low density lipoproteins, even before EPA induced peroxisomal fatty acid oxidation, reduced triglyceride biosynthesis and diminished lipogenesis.
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PMID:The hypotriglyceridemic effect of eicosapentaenoic acid in rats is reflected in increased mitochondrial fatty acid oxidation followed by diminished lipogenesis. 837 81

Hepatocyte growth factor (HGF)/scatter factor is known to be the most potent mitogen for hepatocytes. In this paper, we report that lipogenesis in primary cultured rat hepatocytes treated with 10 ng/ml of recombinant human HGF (rhHGF) for 24 h was stimulated, as measured by the incorporation of 3H2O into long-chain fatty acids, to more than twice as much as the control. Insulin (0.1 microM) was more effective than rhHGF but rhHGF did not show an additive or synergistic effect when added to insulin. We also showed that treatment with rhHGF increased the activities of glucose-6-phosphate dehydrogenase (G6PDH) and malic enzyme, key enzymes which supply NADPH for lipogenesis, and acetyl-CoA carboxylase, the rate-limiting enzyme of lipogenesis. The increase in G6PDH and acetyl-CoA carboxylase activities was accompanied by increases in the levels of mRNA for the enzymes. These results suggest that HGF is involved in liver regeneration not only by stimulation of cell proliferation but also by acceleration of differentiation of hepatocytes.
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PMID:Effect of hepatocyte growth factor/scatter factor on lipogenesis in adult rat hepatocytes in primary culture. 879 95

The time courses of gene expression, and the nutritional regulation of gene expression of lipogenic enzymes (acetyl-CoA carboxylase, fatty acid synthase, ATP citrate-lyase, malic enzyme, and glucose-6-phosphate dehydrogenase) in epididymal adipose tissue after refeeding food-deprived rats have been investigated and compared with those in liver (previously reported). The mRNA concentrations of lipogenic enzymes reached maximum levels at 24 h after the refeeding in adipose tissue and at 8-16 h in liver, while the enzyme induction reached maximum at 48-72 h in both tissues. Moreover, the mRNAs were more strongly induced in adipose tissue than in liver, whereas the enzyme induction (except malic enzyme) was lower. In adipose tissue of rats fed a carbohydrate diet without protein, the mRNA concentrations of acetyl-CoA carboxylase, ATP-citrate lyase, malic enzyme, and fatty acid synthase reached comparable levels to those of the carbohydrate/protein diet group. The protein feeding increased the enzyme induction in adipose tissue. As regards reduction of gene expression, lipogenic enzyme mRNA concentrations were not so markedly reduced by starvation or polyunsaturated fatty acids in adipose tissue as in liver. The differences in regulation of lipogenic enzyme gene expression and induction between adipose tissue and liver can be ascribed to tissue specificity.
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PMID:Nutritional regulation of lipogenic enzyme gene expression in rat epididymal adipose tissue. 888 6

The development of pig adipose tissues is influenced by several factors such as localisation and dietary fat. The neck and backfat subcutaneous adipose tissues consist of two layers with different chemical compositions, and it is not yet known whether such variations are due to differences in lipogenic enzyme activities or to other factors. The aim of the present study was to compare the lipogenic activities of tissues from different sites (Longissimus dorsi muscle, liver, subcutaneous backfat) and between the outer and inner backfat layers. The effects of dietary fat from two animal sources on the lipogenic activities and fatty acid composition of these tissues were also compared. 28 Large White x Pietrain cross-bred swine, averaging 75 (initial) to 108 kg (final) live weight, were allocated into 2 groups. They were fed diets with the same energy and lipid contents but provided either by goat's milk or cow's milk. The lipid content and fatty acid composition of the tissues were determined and the following lipogenic enzymes activities measured: acetyl-CoA carboxylase (CBX); glucose-6-phosphate dehydrogenase (G6PDH) and malic enzyme (ME). Both groups showed similar average daily gain, carcass composition and tissue lipid contents. Lipogenic activities were highest in backfat (p < 0.001), intermediate in Longissimus dorsi muscle and lowest in liver. The lipogenic activities in backfat tissue were greater (p < 0.001) in the inner than in the outer layer in both groups. Animals fed on goat's milk exhibited greater (p < 0.05) CBX and ME activities in the backfat, and CBX (p < 0.05) activity in the Longissimus dorsi muscle. In backfat tissue of animals fed on goat's milk, CBX, G6PDH (p < 0.01) and ME (p < 0.05) were greater in the inner than in the outer layer, whereas in animals fed on cow's milk the inner backfat layer exhibited the slightly higher (p < 0.05) lipid content. Differences in CBX activity between the two dairy diets tended to be greater (p < 0.001) in the inner backfat than in the outer layer. This suggests that the inner layer might be more sensitive to dietary source fat. It is concluded that the layers of pig subcutaneous backfat should not be considered as a single entity, but rather as two separate tissues.
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PMID:Influence of two dairy fats on lipid synthesis in the pig: comparative study of liver, muscle and the two backfat layers. 900 90

Previous studies have shown that the rate of fatty acid synthesis is elevated by more than 20-fold in livers of transgenic mice that express truncated nuclear forms of sterol regulatory element-binding proteins (SREBPs). This was explained in part by an increase in the levels of mRNA for the two major enzymes of fatty acid synthesis, acetyl-CoA carboxylase and fatty acid synthase, whose transcription is stimulated by SREBPs. Fatty acid synthesis also requires a source of acetyl-CoA and NADPH. In the current studies we show that the levels of mRNA for ATP citrate lyase, the enzyme that produces acetyl-CoA, are also elevated in the transgenic livers. In addition, we found marked elevations in the mRNAs for malic enzyme, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase, all of which produce NADPH. Finally, we found that overexpressing two of the SREBPs (1a and 2) led to elevated mRNAs for stearoyl-CoA desaturase 1 (SCD1), an isoform that is detectable in nontransgenic livers, and SCD2, an isoform that is not detected in nontransgenic livers. This stimulation led to an increase in total SCD activity in liver microsomes. Together, all of these changes would be expected to lead to a marked increase in the concentration of monounsaturated fatty acids in the transgenic livers, and this was confirmed chromatographically. We conclude that expression of nuclear SREBPs is capable of activating the entire coordinated program of unsaturated fatty acid biosynthesis in mouse liver.
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PMID:Nuclear sterol regulatory element-binding proteins activate genes responsible for the entire program of unsaturated fatty acid biosynthesis in transgenic mouse liver. 985 71


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