We investigated the effects of dietary folate supplementation on plasma homocysteine, vitamin B$_{12}$ and hepatic levels of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) in diet-induced hyperhomocysteinemic rats. All animals were fed 0.3% homocysteine diet for 2 weeks, then they were placed either on a 0.3% homocystine or no homocystine with or without 8 mg/kg folate diet for 8 weeks. Homocystine diet induced hyperhomocysteinemia up to 3.5-fold at 10 weeks (28.0 $\pm$ 4.8 $\mu$mol/l vs. 7.9 $\pm$ 0.3 $\mu$mol/l). Dietary folate supplementation caused a significant decrease in plasma homocysteine levels which had been increased by a homocystine-diet. Also, dietary folate supplementation made them return to control levels at 4 wk when the diet was free of homocystine. Plasma folate levels were markedly decreased with homocystine diet with no folate supplementation. Plasma vitamin B$_{12}$ did not differ between groups. Dietary homocystine increased hepatic levels of SAM in folate supplementation group at 10 weeks (p<0.05). Dietary folate supplementation increased hepatic levels of SAM/SAH ratios in homocystine group (p<0.05). In conclusion, dietary folate supplementation can effectively ameliorate the detrimental effects of hyperhomocysteinemia.mia.
Chronic alcohol consumption is associated with perturbation of hepatic metabolism of sulphur-containing amino acid. The goal of present study was to evaluate the influence of dietary supplementation of methionine or folate to chronically ethanol-fed mts on the metabolism of sulfur-containing amino acids and one-carbon metabolism. Sprague-Dawley male mts were fed Lieber-Decarli liquid diet with 0% ethanol (control), 36% ethanol (E), 36% ethanol combined with methionine supplement (EM) or folate supplement (EF) for 8 weeks. Hepatic S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), plasma folate and homocysteine (Hcy), urinary excretion of folate and formiminoglutamate were investigated after feeding experimental diets. Growth was retarded by 36% ethanol consupmtion (E, EM and EF) (p<0.01). Liver total fat (p<0.05) and plasma ALT (P<0.01) were increased by methionine supplementation (EM), implicating fatty liver and liver injury. Liver folate was increased slightly by folate supplementation (EF) (p=0.077). Urinary folate loss was increased 2.3 fold by ethanol consumption (E) and 17.2 fold by folate supplementation (EF), while decreased by methionine supplementation (EM) (p<0.000l). Plasma Hcy was increased 1.9 fold by methionine supplementation (EM) in ethanol-fed mts (p<0.05), which was related with decreased methionine synthase activity (p<0.05). Hepatic SAM/SAH ratio was depressed by methionine supplementation in ethanol-fed mts (EM) (p<0.05). Urinary formininoglutamate (Figlu) excretion after histidine loading was increased by ethanol ingestion and reduced by methionine supplementation (p<0.00l). Based on these data, methionine supplementation appears to accelerate histidine oxidation. In conclusion, dietary supplementation of methionine to ethanol-fed mts exacerbates alcoholic liver injury possibly by complicating sulphur-containing amino acid metabolism, as while it may have beneficial effects on folate and histidine metabolism.
In patients with type 2 diabetes, oxidative stress could be increased by their metabolic changes. Elevated plasma homocysteine is considered as one of markers of enhanced oxidative stress. Due to oxidative stress, some complications like cardiovascular or renal diseases may develop in type 2 diabetes patients. Plasma homocysteine concentration may be increased if folate status were inadequate. Protective effects against oxidative stress may be diminished if the status of anti-oxidative nutrient as vitamin C was poor. It is, therefore, important to maintain adequate status of folate and vitamin C in type 2 diabetes patients. Thus, this study was performed to determine the effects of supplementation of folate and/or ascorbate on blood glycated hemoglobin ($HbA_{1c}$) level, serum concentrations of homocysteine and cholesterol, plasma oxidized low density-lipoprotein (LDL), concentration and plasma glutathione peroxidase (GSH-Px) activity in the patients with type 2 diabetes. A total of 92 type 2 diabetes patients participated voluntarily with written consents. They were divided into one of the four experimental groups; Control (C), Folate-supplemented (F), Ascorbate-supplemented (A), and Folate plus ascorbate-supplemented (FA). The subjects in C were taken placebo, those in F were supplemented 1 mg of folate, those in A received 1,000 mg of ascorbate, and those in FA were given 1 mg of folate plus 1,000 mg of ascorbate daily for 4 weeks. Supplementation of folate or ascorbate resulted to increase serum folate level or plasma ascorbate concentration apparently, respectively. Folate supplementation not ascorbate seemed to decrease plasma concentrations of homocysteine and oxidized LDL and reduce plasma GSH-Px activity. There might not be synergic effect of the supplementation of folate plus ascorbate. The results indicate that oxidative stress in the patients with type 2 diabetes may lower mainly by folate supplementation.
Chronic abuse of alcohol can lead to the development of folate deficiency due to inadequate folate intaike, excessive urinary excretion and from effects of ethanol on folate absorption and metabolism . To investigate the effects of alcohol and folate intake on folate metabolism, the rates were raised for 4 and 10 weeks on experimental diets containing 0, 2 8mg folate/kg diet, and were administered 50% ethanol(1.8$m\ell$/kg body weight) three times a week intragastrically. Plasma and tissue folate concentrations were found to be significantly influenced by dietary folate level. In animals fed on folate-deficient diet, concentrations of folate in the plasma, liver and kidney were decreased by 60-89% compared to those on folate-adequate diet, and ther values were further decreased with experimental period. Folate supplementation increased plasma and tissue folate levels significantly by 16-78% compared to those on folate-adequate diet, and the folate levels in the plasma and liver were affected most by the supplementation. Alcohol administration did not seem to influence folate status in the body significantly when animals were raised on folate-deficient diet. However, when rats were fed folate-adequate or folate-supplemented diet, alcohol was shown to decrease plasma and tissue folate concentrations. Among the animals receiving alcohol, folate concentrations in the plasma and tissues were significantly higher when animals fed folate-supplemented diet compared to folate adequate diet. Alcohol seems to exert differential effects on urinary foalte excretion by experimental period it increased urinary folate in the 4-week period, but lowered foalte excretion in the urine when the experimental period was extended to 10 weeks. Alcohol did not seem to influence folate excretion in the feces. These results indicate that folate supplementation might be beneficial in ameliorating the inadequate folate status that might occur with chronic alcoholism.
The critical role of folate vitamin in the remethylation pathway for methionine synthesis from homocysteine has been well documented. Hyperhomocysteinemia resulting from inadequate folate nutrition has been implicated in increased incidence of macrovascular diseases, colorectal cancer, neural tube defects, etc. Chronic exposure to ethanol impairs folate nutrition and one-carbon metabolism in the liver, which often results in fatty liver due to a defective remethylation process. This study was carried out to investigate the chronic effects of moderate levels of alcohol and dietary 131ate on plasma homocysteine levels, and on histopathology and biochemical functions of the liver Rats were raised on experimental diets with three levels of folate(0, 2, 8mg/kg diet), and 50% ethanol(1.8m1/kg body weight) was administered intragastrically by intubation tubes three times a week for 10 weeks. Plasma homocysteine concentrations were found to be significantly influenced by dietary folate intake and alcohol administration. Among all treatment groups, Plasma homocysteine levels were highest in the animals receiving a combined treatment of folate deficient diet and alcohol administration. Plasma homocysteine concentration was negatively correlated with folate concentration in the plasma(p<0.01) and liver(p<0.05). Among alcohol treated rats, increase in plasma homocysteine values due to ethanol was prevented by 131ate supplementation. When liver histological tests were performed, macrovascular and microvascular fatty changes and spotted necrosis were observed more frequently in folate-deficient animals diet than those on folate-adequate and folate-supplemented diets in alcohol-treated rats. These results indicate that folate supplementation above the recommended level might be beneficial in the prevention of alcohol-related hyperhomocystei-nemia and abnormal histologic changes in the liver due. (Korean J Nutrition 31(7) : l121-l129, 1998)
The purpose of the present study was to measure the dietary folate intake of Korean women of childbearing age. Folate intake obtained from 24-hour recall method and food frequency questionnaire was assessed in two hundred and ninety-three nonpregnant and non-lactating healthy women of childbearing age. The mean folate intake of women aged 20-29 was 112.8ug/day, 49.3% of their recommended level of 250ug/day. Folate intake of women aged 30-49 was 129.0ug/day, significantly higher than that of participants aged 20-29. A quartile analysis on the folate intake revealed that there significant differences in the consumption of dark green, leafy vegetables (p<0.01), other vegetables (p<0.01), and fruits and legumes(p<0.05) between the highest of childbearing age is far from adequate. To reach of the present study show that the folate intake of Korean women of childbearing age is far from adequate. To reach the recommended intake level of 250ug/day for women of childbearing age, folate supplementation and special nutrition education promoting folate intake might be necessary.
Hyperhomocysteinemia, resulted from an interaction between the mutation of MTHFR gene and B vitamin deficiency, is suggested as a possible cause for complications and adverse outcomes of pregnancy. The purpose of the present study was to investigate the relationship between the intakes of B vitamins and serum homocysteine concentrations with the C677T mutation in the MTHFR genotypes in 135 normal pregnant women of 24-28 weeks of gestation. Dietary intake of B vitamins did not differ among the three genotypes, but the negative correlation between dietary folate intake and the serum homocysteine level was the strongest in the T/T type (r = -0.249) than in other genotypes (C/T: r= -0.040, C/C:r= 0.126, p<0.05). Among the subject with the T/T type, the pregnant women who consumed folate less than 50% of the RDA had higher serum homocysteine levels than those who consumed folate greater than 125% of the RDA (10.4$\pm$5.9 vs 7.0$\pm$1.5 $\mu$mol/L, p<0.05). Serum homocysteine levels were higher in the women with micronutrient supplements than those with no supplements in the T/T type, but such relation was not present in the C/C or the C/T type. In conclusion, serum homocysteine concentrations were influenced by the interrelationship between the MTHFR polymorphisms and dietary folate intake or micronutrient supplementation.
This study was performed to investigate the effect of vitamin C and E supplementation on blood pressure, plasma lipids, folate, and homocysteine levels in smokers and non-smokers of college male students in Gyeonggi Area. The nutrient intakes were determined by a 24hr-recall method. The subjects were divided into six groups: vitamin C sup-plementation group (n: smokers = 10, nonsmokers = 10), vitamin E supplementation group (n: smokers = 10, nonsmokers = 10), vitamin C and E supplementation group (n: smokers = 10, nonsmokers = 10), respectively. There were no significant differences between the smokers and nonsmokers in terms of anthropometric measurements. Systolic and diastolic blood pressure were significantly higher (p < 0.05) in smokers than that of non-smokers. There was no significant difference in energy and other nutrients intakes between smokers and non-smokers. In plasma lipids levels, smokers had higher plasma triglyceride, LDL-cholesterol, VLDL-cholesterol, total cholesterol concentration than that of non-smokers (p < 0.05). HDL-cholesterol level of smokers had a tendency to be lower than that of non-smokers. In smokers, AI, TPH, LPH were significantly higher than that of non-smokers (p < 0.01). Plasma folate, homocysteine levels were not significantly different between smokers and non-smokers. The effect of antioxidant vitamins supplementation in smokers: In vitamin C supplementation group, HDL-cholesterol level was significantly in-creased (p < 0.01) and AI, TPH, LPH were significantly decreased (p < 0.01). In vitamin E supplementation group, HDL-cholesterol level was significantly increased (p < 0.05). In vitamin C and E supplementation group, LPH was significantly decreased (p < 0.05). The effect of antioxidant vitamins supplementation in non-smokers: HDL-cholesterol level was significantly increased (p <0.05) and AI, TPH, LPH were significantly decreased (p <0.05) by vitamin C supplementation group. Plasma homocysteine level was decreased by vitamin E supplementation group in non-smokers (p < 0.01). The results of this study showed that smoking had a tendency to increase plasma lipids levels that factor into the risk of coronary heart disease. It is considered that antioxidant vitamin supplementation in smokers had a tendency to decrease cardiovascular disease than in nonsmokers.
Folate is generally considered as a safe water-soluble vitamin for supplementation. However, we do not have enough information to confirm the potential effects and safety of folate supplementation and the interaction with vitamin $B_{12}$ deficiency. It has been hypothesized that a greater methyl group supply could lead to compensation for vitamin $B_{12}$ deficiency. On this basis, the present study was conducted to examine the effects of high-dose folic acid (FA) supplementation on biomarkers involved in the methionine cycle in vitamin $B_{12}$-deficient rats. Sprague-Dawley rats were fed diets containing either 0 or $100{\mu}g$ (daily dietary requirement) vitamin $B_{12}/kg$ diet with either 2 mg (daily dietary requirement) or 100 mg FA/kg diet for six weeks. Vitamin $B_{12}$-deficiency resulted in increased plasma homocysteine (p<0.01), which was normalized by dietary supplementation of high-dose FA (p<0.01). However, FA supplementation and vitamin $B_{12}$ deficiency did not alter hepatic and brain S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) concentrations and hepatic DNA methylation. These results indicated that supplementation of high-dose FA improved homocysteinemia in vitamin $B_{12}$-deficiency but did not change SAM and SAH, the main biomarkers of methylating reaction.
Lactating women have an increased need of folate in the breastfeeding period and, as a consequence, may be in risk of folate deficiency. Folate content of breast milk, furthermore, is important for infants to support exponential growth. However, little is known about the folate content of breast milk from Korean lactating women and their folate nutritional status. In this study, therefore, we investigated the folate status of Korean lactating women and the folate content of their breast milk during extended lactation. A total of 10 subjects who delivered full-term infants participated this study voluntarily. Dietary folate intakes were measured and blood and breast milk were collected at 1, 2, 3, and 6 months postpartum. The women who did not take folic acid supplements failed to meet the recommended intake(RI) of folate for lactating women during all the study periods but those who did met the RI. The unsupplemented women showed lower plasma folate concentrations compared to the supplemented women and all the women were in suboptimal folate status determined by plasma folate concentration throughout the study periods. But the supplemented women showed lower prevalence of suboptimal folate status only at 3 or 6 months postpartum. Plasma folate concentrations of both groups decreased with the progression of lactation. Erythrocyte folate concentrations were not different between the two groups, however, that of the unsupplemented reduced further as time progressed. Plasma homocysteine levels were not different between the two groups. Concentrations of erythrocyte folate and plasma homocysteine were not changed throughout the study periods. Folate contents of their breast milk through the study periods were not different between the two groups and it decreased as lactation progressed in both groups. The results of this study suggest that the folate nutritional status of Korean lactating women might be deteriorated with the progression of lactation without folic acid supplements.
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