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

The activity of several enzymes of regulatory importance for the pathways of glycolysis, gluconeogenesis and lipogenesis was investigated in the placenta and liver of pregnant rats and in the liver of non-pregnant female rats. The rats received daily hormonal treatments on Days 15 to 17 of pregnancy and enzyme activities were measured on Day 18. Chorionic gonadotropin induced minor changes in enzyme activity, apart from a decrease in the activity of hepatic enzymes of lipogenesis in non-pregnant rats. Triamcinolone induced a marked increase in enzymes of gluconeogenesis and a decrease in the activity of pyruvate kinase in the liver of pregnant and non-pregnant rats; in contrast, inverse changes in activity, these enzymes were observed in the placenta. This response in the placenta was considered to arise not from direct hormone effect, but from the accompanying hyperglycemia and hyperinsulinemia. Triamcinolone also increased the activity of hepatic acetyl-CoA carboxylase in pregnant and non-pregnant rats, whereas it reduced the activity of this enzyme in the placenta. Estrogen produced changes similar to those of triamcinolone in the liver and placenta, except that it depressed the activity of acetyl-CoA carboxylase in both tissues. Progesterone had little effect on placental and hepatic enzymes. In general, the changes induced by these hormones in the placenta affected fewer enzymes than in the liver, were less extensive in magnitude and not necessarily in the same direction as in the liver. This indicates that the regulatory placental enzymes are subject to specific control mechanisms not necessarily influenced by direct hormone action.
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PMID:Effect of chorionic gonadotropin, triamcinolone, progesterone and estrogen on enzymes of placenta and liver in rats. 23 7

Insulin stimulates lipogenesis by 100% for 5 h by a covalent modulation of acetyl-CoA carboxylase, and by 200% for 24 h by increasing malic enzyme and fatty acid synthase enzymic activities in brown-adipocyte primary cultures. At short times, noradrenaline and isoprenaline decrease lipogenesis. However, phenylephrine and glucagon have no effect. At long times, dexamethasone inhibits lipogenesis. This effect is precluded in the presence of insulin. Progesterone and tri-iodothyronine, alone or in the presence of insulin, produce a stimulation of the rates of lipogenesis.
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PMID:Hormonal regulation of rat foetal lipogenesis in brown-adipocyte primary cultures. 304 67

In fetal lung the amounts of mRNAs encoding fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) and ATP citrate lyase (ACL) increase in late gestation and drop around birth. To study the mechanism of the perinatal decrease, pregnancy was prolonged from 22 (term) to 25 days in rats with daily injections of progesterone. Progesterone did not affect the levels of lipogenic enzyme mRNAs in fetal lung prior to term, but significantly delayed the perinatal decrease in the levels of lung FAS and ACC mRNA. Although for ACL mRNA abundance the differences were not statistically significant, its pattern in the control and progesterone groups were similar to those of FAS and ACC mRNA. Malic enzyme mRNA did not change between 20 and 25 days after conception in either group. These results suggest that the decrease in FAS and ACC mRNA at term can be partially explained by labor, delivery, air-breathing or switch from carbohydrate to fat metabolism.
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PMID:Gene expression of fatty acid synthesizing enzymes in fetal rat lung in prolonged pregnancy. 853 72