Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.2.1.22 (cystathionine beta-synthase)
 965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The experiments described here were set up (a) to investigate the effect of age and (b) to investigate the effect of giving five diets which varied in methionine and choline or betaine contents on some of the enzymes that metabolize these nutrients in chick liver. Growth and carcass composition of the chicks fed on the different diets were also examined. There was no obvious relationship between age and enzyme activity in young chicks. Only a diet low in methionine (but not one low in choline) showed a significant decrease in growth and a change in carcass composition. The effects of diet on enzyme activity were complex. Choline oxidase (EC 1.1.3.17) activity was affected by the level of choline in the diet, being high when choline was present at high levels, especially when methionine was limiting. 5-Methyltetrahydrofolate homocysteine methyltransferase (EC 2.1.1.3) had a high activity in the livers of chicks fed on a conventional diet compared with those given semi-purified diets. Other enzymes showed minor changes in response to the diet. The diet low in methionine showed a lower activity of cystathionine beta-synthase (EC 4.2.1.22) and slightly higher activities of methionine adenosyltransferase (EC 2.5.1.6) and betaine-homocysteine methyltransferase (EC 2.1.1.5; compared with other diets), suggesting that this diet encouraged re-methylation of homocysteine at the expense of trans-sulphuration to cystathionine. The findings obtained in these studies form a useful basis for further investigation of the metabolic interrelationships between methionine and related nutrients.
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PMID:Changes in body-weight, composition and hepatic enzyme activities in response to dietary methionine, betaine and choline levels in growing chicks. 169 35

The effect of vitamin B12(B12)-deficiency on the activities of hepatic methionine synthase, homocysteine methyltransferase, and cystathionine beta-synthase was investigated in rats. The rats bred from B12-deficient dams were fed the B12-deficient diets for 150 days after weaning. Growth retardation of the B12-deficient rats was already observed on day 30 and continued through 150 days. But dietary supplementation of 0.5% DL-methionine slightly improved the growth retardation. Urinary excretion of methylmalonic acid increased to about 15 mg/mg creatinine and hepatic B12 concentration declined to about 2 ng/g liver after a 150-day feeding of the B12-deficient diets. Hepatic methionine synthase activity in rats fed the B12-deficient diets supplemented with or without methionine decreased to about 5% of B12-supplemented controls. Hepatic betaine-homocysteine methyltransferase activity showed no significant change caused by B12-deficiency. Hepatic cystathionine beta-synthase activity in rats fed the B12-deficient diets supplemented with or without methionine decreased to about 61% and 27% of their B12-supplemented controls, respectively, but the decrease was partially improved by methionine supplementation. In conclusion, the rats bred from B12-deficient dams showed a severe B12-deficiency after a 150-day feeding of the B12-deficient diets. The decrease of hepatic cystathionine beta-synthase activity was supposed to be due to the adaptation by the defect of methionine resynthesis.
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PMID:Effect of vitamin B12-deficiency on the activity of hepatic cystathionine beta-synthase in rats. 273 4

The activities of choline oxidase and betaine-homocysteine methyltransferase increased markedly in pre-ruminant lamb liver after birth and subsequently decreased when the lambs reached the ruminant state, while the developmental changes in hepatic 5-methyl-H4folate-homocysteine methyltransferase were negatively correlated with those of betaine-homocysteine methyltransferase. Hepatic phospholipid methyltransferase was elevated almost four-fold by the 10th postnatal day, but declined thereafter. Hepatic glycine methyltransferase in one-day-old lambs increased 55-fold, compared with that of fetuses, and thereafter decreased dramatically with age. Guanidoacetate methyltransferase, glycine methyltransferase and betaine-homocysteine methyltransferase in sheep pancreas increased markedly with age and were many times higher than the hepatic enzymes in adult sheep. Choline oxidase, betaine-homocysteine methyltransferase, cystathionine beta-synthase and glycine methyltransferase in adult sheep liver were much lower than those in rat. These results illustrate the conservative features of methyl group metabolism in postruminant sheep.
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PMID:Developmental changes in the activities of enzymes related to methyl group metabolism in sheep tissues. 351 Aug 9

The effect of lactation on a number of enzymes involved in transmethylation reactions and the secretion of major methyl compounds into milk have been examined in sheep. The activities of hepatic phospholipid methyltransferase and 5-methyltetrahydrofolate-homocysteine methyltransferase were significantly higher in lactating ewes, compared with those in non-lactating ewes, while the activity of both hepatic and pancreatic glycine methyltransferase was significantly lower in the lactating state. No differences were observed in the activities of hepatic guanidoacetate methyltransferase, betaine-homocysteine methyltransferase and cystathionine beta-synthase on lactation. These results suggest that the extra demand for methyl groups for the secretion of methyl compounds in the milk is facilitated by enhancing the rate of de novo methyl group synthesis and lowering the rate of physiologically nonessential methylation.
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PMID:Regulation of methyl group metabolism in lactating ewes. 406 54

The hepatic enzyme glycine N-methyltransferase (GNMT) plays a major role in the control of methyl group and homocysteine metabolism. Because disruption of these vital pathways is associated with numerous pathologies, understanding GNMT control is important for evaluating methyl group regulation. Recently, gluconeogenic conditions have been shown to modulate homocysteine metabolism and treatment with glucocorticoids and/or all-trans-retinoic acid (RA)-induced active GNMT protein, thereby leading to methyl group loss. This study was conducted to determine the effect of diabetes, alone and in combination with RA, on GNMT regulation. Diabetes and RA increased GNMT activity 87 and 148%, respectively. Moreover, the induction of GNMT activity by diabetes and RA was reflected in its abundance. Cell culture studies demonstrated that pretreatment with insulin prevented GNMT induction by both RA and dexamethasone. There was a significant decline in homocysteine concentrations in diabetic rats, owing in part to a 38% increase in the abundance of the transsulfuration enzyme cystathionine beta-synthase; treatment of diabetic rats with RA prevented cystathionine beta-synthase induction. A diabetic state also increased the activity of the folate-independent homocysteine remethylation enzyme betaine-homocysteine S-methyltransferase, whereas the activity of the folate-dependent enzyme methionine synthase was diminished 52%. In contrast, RA treatment attenuated the streptozotocin-mediated increase in betaine-homocysteine S-methyltransferase, whereas methionine synthase activity remained diminished. These results indicate that both a diabetic condition and RA treatment have marked effects on the metabolism of methyl groups and homocysteine, a finding that may have significant implications for diabetics and their potential sensitivity to retinoids.
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PMID:Modulation of methyl group metabolism by streptozotocin-induced diabetes and all-trans-retinoic acid. 1534 42

Numerous perturbations of methyl group and homocysteine metabolism have been documented as an outcome of diabetes. It has also been observed that there is a transition from hypo- to hyperhomocysteinemia in diabetes, often concurrent with the development of nephropathy. The objective of this study was to characterize the temporal changes in methyl group and homocysteine metabolism in the liver and kidney and to determine the impact these alterations have on DNA methylation in type 1 diabetic rats. Male Sprague-Dawley rats were injected with streptozotocin (60 mg/kg body weight) to induce diabetes and samples were collected at 2, 4, and 8 wk. At 8 wk, hepatic and renal betaine-homocysteine S-methyltransferase activities were greater in diabetic rats, whereas methionine synthase activity was lower in diabetic rat liver and kidney did not differ. Cystathionine beta-synthase abundance was greater in the liver but less in the kidney of diabetic rats. Both hepatic and renal glycine N-methyltransferase (GNMT) activity and abundance were greater in diabetic rats; however, changes in renal activity and/or abundance were present only at 2 and 4 wk, whereas hepatic GNMT was induced at all time points. Most importantly, we have shown that genomic DNA was hypomethylated in the liver, but not the kidney, in diabetic rats. These results suggest that diabetes-induced perturbations of methyl group and homocysteine metabolism lead to functional methyl deficiency, resulting in the hypomethylation of DNA in a tissue-specific fashion.
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PMID:Type I diabetes leads to tissue-specific DNA hypomethylation in male rats. 1893 99

To determine the effect of dietary protein level on experimental hyperhomocysteinemia, rats were fed 10% casein (10C) and 40% casein (40C) diets with or without 0.5% guanidinoacetic acid (GAA) for 14 d. In addition, rats were fed 10C + 0.75% methionine (10CM) and 40C + 0.75% methionine (40CM) diets with or without 2.5% serine for 14 d to determine the relationship between the dietary protein level and intensity of the hypohomocysteinemic effect of serine. GAA supplementation markedly increased the plasma homocysteine concentration in rats fed with the 10C diet, whereas it did not increase the plasma homocysteine concentration in rats fed with the 40C diet. Although serine supplementation significantly suppressed the methionine-induced enhancement of plasma homocysteine concentration, the decreased plasma homocysteine concentration was significantly lower in rats fed with the 40CM diet than in rats fed with the 10CM diet. The hepatic cystathionine beta-synthase and betaine-homocysteine S-methyltransferase activities were significantly higher in rats fed with the 40C or 40CM diet than in rats fed with the 10C or 10CM diet, irrespective of supplementation with GAA and serine. These results indicate that the high-casein diet was effective for both suppressing GAA-induced hyperhomocysteinemia and potentiating the hypohomocysteinemic effect of serine, probably through the enhanced activity of homocysteine-metabolizing enzymes.
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PMID:High-casein diet suppresses guanidinoacetic acid-induced hyperhomocysteinemia and potentiates the hypohomocysteinemic effect of serine in rats. 1906 Apr 1

To clarify the relationship between dietary choline level and plasma homocysteine concentration, the effects of choline deprivation on plasma homocysteine concentration and related variables were investigated in rats fed a standard (25%) casein (25C) diet or standard soybean protein (25S) diet. Using the 25S diet, the time-dependent effect of choline deprivation and the comparative effects of three kinds of lipotropes were also investigated. Feeding rats with the choline-deprived 25S diet for 10 d significantly increased plasma total homocysteine concentration to a level 2.68-times higher than that of the control group, whereas choline deprivation had no effect in rats fed the 25C diet. Increases in hepatic S-adenosylhomocysteine and homocysteine concentrations, decreases in hepatic betaine concentration and the activity of cystathionine beta-synthase, but not betaine-homocysteine S-methyltransferase, and fatty liver also occurred in rats fed the choline-deprived 25S diet. Plasma homocysteine concentration increased when rats were fed the choline-deprived 25S diet for only 3 d, and the increase persisted up to 20 d. The hyperhomocysteinemia induced by choline deprivation was effectively suppressed by betaine or methionine supplementation. Choline deprivation caused hyperhomocysteinemia also in rats fed a choline-deprived low (10%) casein diet. The results indicate that choline deprivation can easily induce prominent hyperhomocysteinemia when rats are fed relatively low methionine diets such as a standard soybean protein diet and low casein diet, possibly through the suppression of homocysteine removal by both remethylation and cystathionine formation. This hyperhomocysteinemia might be a useful model for investigating the role of betaine in the regulation of plasma homocysteine concentration.
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PMID:Choline deprivation induces hyperhomocysteinemia in rats fed low methionine diets. 1915 87

Experiments were conducted to clarify the relationship between dietary protein level and plasma homocysteine concentration in rats. Male Wistar rats were fed diets differing in casein level from 5 to 50% for 14 d (Expt. 1). Plasma total homocysteine concentration was positively correlated with dietary casein level in the range of 5 to 10% but inversely correlated with dietary casein level in the range of 10 to 50%. Hepatic cystathionine beta-synthase (CBS) and betaine-homocysteine S-methyltransferase (BHMT) activities and renal CBS activity increased in response to dietary casein level in the range of 10 to 50%, whereas hepatic serine and betaine concentrations decreased with increasing dietary casein levels. When rats were fed the 10% casein diet or 10% casein+17.2% amino acid mixture diet for 14 d, plasma homocysteine concentration was significantly lower in rats fed the amino acid mixture-added diet than in rats fed the 10% casein diet (Expt. 2), indicating that the hypohomocysteinemic effect of high casein diets was elicited by amino acids, not by casein contaminants. The degree of increase in plasma homocysteine concentration caused by dietary supplementation with 0.75% L-methionine was significantly lower in rats fed the 40% casein diet than in rats fed the 10% casein diet (Expt. 3). These results indicate that high casein diets do not increase but rather decrease plasma homocysteine concentration and cause resistance to hyperhomocysteinemic treatment, and suggest that such effects of high casein diets are mediated at least by increased activities of CBS and BHMT.
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PMID:High casein diet decreases plasma homocysteine concentration in rats. 1935 60

Rats were fed diets with and without 0.5% L-cysteine supplement for 14 d or shorter periods to clarify the mechanism by which dietary cysteine elicits its hypohomocysteinemic effect. Cysteine supplementation significantly decreased plasma homocysteine concentration with an increase in plasma cysteine concentration in rats fed 10% casein diet (10C) or 15% soybean protein diet (15S) but not in rats fed 25% casein diet (25C) or 25% soybean protein diet. Cysteine supplementation also significantly suppressed hyperhomocysteinemia induced by choline-deprived 10C with an increase in plasma cysteine concentration but not that induced by 25C+0.65% methionine or 25C+0.4% guanidinoacetic acid. Hepatic S-adenosylmethionine (SAM) and homocysteine concentrations were significantly decreased by cysteine supplementation of 15S. These decreases in plasma homocysteine concentration and hepatic SAM and homocysteine concentrations due to cysteine supplementation disappeared when 15S was fortified with 0.3% methionine. The plasma homocysteine concentration significantly decreased with an increase in plasma cysteine concentration only 1 d after diet change from 15S to cysteine-supplemented 15S, while hepatic cystathionine beta-synthase and betaine-homocysteine S-methyltransferase activities were not altered. Unlike cysteine, cysteic acid and 2-mercaptoethylamine did not decrease plasma homocysteine concentration. These results indicate that cysteine markedly decreases plasma homocysteine concentration only when added to diets low in both protein and methionine levels and suggest that increased plasma cysteine concentration and decreased flow of methionine toward homocysteine formation, but not alteration of homocysteine-metabolizing enzyme activities, are associated with the hypohomocysteinemic effect of cysteine.
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PMID:Hypohomocysteinemic effect of cysteine is associated with increased plasma cysteine concentration in rats fed diets low in protein and methionine levels. 1935 65


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