Folate coenzymes are involved in one-carbon transfer reactions needed for the synthesis of nucleic acids, amino acids, and proteins which are very important for cell proliferation and differentiation. To investigate the effects of dietary folate content on plasma and tissue folate concentrations and on folate excretions in urine and feces, male Sprague-Dawley rats were raised for 4-10 weeks on semi-purified experimental diets containing 0mg, 2 mg, 8mg folate/kg diet. Folate concentrations were determined microbiologically using Lactobacillius casei (ATCC 7469). When compared to the folate adequate diet, the folate deficient diet decreased folate levels in plasma, liver and kidney , and the values were further decreased with experimental period. In rats reviving folate supplemented diets, plasma , liver and kidney folate adequate or supplemented diets, folate concentrations weer increased compared to animals on the folate adequate diet. In the folate adequate or supplemented diets, folate concentrations in the plasma and kidney were maintained at essentially the same level for 10 weeks . Folate concentrations in the liver, however, continued to increase with experimental period. Dietary folate intake seems to influence plasma and liver folate concentrations more than kidney folate concentrations. Folate excretions unrine and feces were significantly increased with dietary foalte intakes and experimental period. Folate excreted via urine was consideerably greater than that via feces. These resutls indicated that the foate supplemented diet improved plasma and tissue foalte status. Whether folate supplmentation improves foalte-dependent reactions remains to be researched.
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.
Journal of the Korean Society of Food Science and Nutrition
/
v.26
no.5
/
pp.983-992
/
1997
During pregnancy and lactation, folate status is important because folate requirements increase during the periods as well as maternal folate status influences on pregnancy outcome and human milk folate; especially folate deficiency around periconceptional period may induce neural tube defects(NTDs) of fetus. There have been a plenty of evidences that maternal folate status deteriorates during pregnancy of fetus. There have been a plenty of evidences that maternal folate status deteriorates during pregnancy and lactation if folate needed is not sufficiently provided. The Public health Service of the United States recommends all child-bearing is not sufficiently provided. The Public Health Service of the United States recommends all child-bearing women to intake 0.4mg of folate daily, and the Food and Drug Administration the folate status of child-bearing women and to reduce the rate of occurrence of NTDs. Many authors have insisted that the current recommended dietary allowances of folate for Americans are too low to maintain good folate status. There are little data about Korean folate status including pregant and lactating women. A couple of reports indicated that the folate intakes of Korean pregant and lactating women are below the Korean RDAs of folate and serum folate levels of them are subnormal. The authors pregnant and lactating women. Therefore, it is worth to review the assessment methods of folate status of pregnant and lactating women, folate RDAs for them, the relationships between maternal folate status and pregnancy outcome as well as human milk folate, the methods to increase folate intake, and the problems of large dose of folic acid supplementatiion.
The effect of 9-methyl folate on histidine oxidation, the uptake of an injected dose of $[^{3}H]folate$ by the livers and kidneys, the hepatic and blood folate levels were investigated by feeding crude x-methyl folate(XMF) at a level of 5 g per kg diet. 9-Methyl folate is konwn as a major forate antagonist in XMF to produce deficiency signs in rat. Feeding of XMF decreased histidine oxidation and hepatic folate levels significantly, which showed the function of 9-methyl folate as an antifolate in rats. The hepatic uptake of labeled folate in XMF- fed rats was decreased significantly. These data led to conclude that 9-methyl folate inhibited folate uptake and retention by tissue, especially liver, which could explain the low liver folate levels and the decreased histidine oxidation. However, only very low level of 9-methyl folate was detected in liver. It suggested that 9-methyl folate may be metabolized very quickly in the liver after uptaken.
Folate, a precursor of the coenzyme tetrahydrofolate, plays an important role in DNA replication and cell proliferation, and thus could influence rapidly proliferating immune cells such as leukocytes and splenocytes. The effects of dietary folate on folate concentrations of plasma, thymus, spleen and leukocytes were investigated in rats. The animals were raised for 6 weeks on semipurifed experimental diets containing 0mg, 2mg, 4mg, 8mg folate/kg diet. Folate concentrations were determined microbiologically using Lactobacillus casei(ATCC 7469), and DNA strand breaks produced by alkaline treatment were analyzed fluorometrically. When compared to folate adequate diet, the folate deficient diet(0mg folate/kg diet) resulted in lowest folate levels in plasma, thymus, spleen and leukocytes, and the highest DNA strand breaks in spleen cells and leukocytes. Dietary folate levels significantly increased folate concentrations of immune tissues, leukocytes, and the plasma in a dose dependent manner, folate concentrations being highest with a diet providing 8mg folate/kg diet. The percentages of the double strand DNA remaining in the splenocytes and leukocytes after alkaline treatment were significantly increased with higher amounts of dietary folate in a dose dependent manner. Folate intakes of 8mg than 4mg/kg diet was found to be more effective in the prevention of DNA strand breaks. The results of this study suggest that increased folate above the requirement level could improve DNA stabilities in immune cells.
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.
Microbiological method using a 96-well microplate reader for folate assay was established, and folate intake and blood folate concentrations of 23 female college students were assessed. To evaluate folate intake, dietary data were collected by a 3-day weight food record, and serum and RBC folate concentrations were measured by the new method. The coefficient of variation for the new method was less than 10%. Mean daily folate intake of the subjects was 126.7${\mu}g$ which is only 50.7% of the RDA. The mean concentrations of serum and RBC folate were 7.46ng/ml and 294.4ng/ml, respectively, which were within the normal range. These results indicate that folate intake seems to be underestimated due to incomplete food composition database. Therefore, folate database should be appropriately in order to asses folate intake accurately.
Dietary folate intake and serum folate levels were measured in 26 pregnant, 25 lactating, and 17 non-pregnant, non-lactating women. Dietary folate comsumption was estimated by calculating folate intake based on the information obtained from food frequency quesionnaires and serum folate levels were determined microbiologically using Lactobacillus casei. The total folate (from food and supplements) intakes of pregnant and lactating women were 326.9ug and 407.9ug, which was significantly higher than that of the non-pregnant, non-lactating women(139.5ug). However, with regard to food folate intake, there were no differences among the three groups (160ug for pregnant women, 143.4ug for lactating women). Forty-two percent and 36% of the pregnant and lactating subjects, respectively, were found to be taking commercially available nutritional supplements containing folate. The concentrations of folate in these supplements were in the range of 83ug~1, 000ug per tablet. For lactating women, serum folate levels were significantly higher when folate supplements were voluntarily used. The amount of folate intake was positively correlated with the serum folate levels in pregnant women, but not in lactaing women and non-pregnant, non-lactating women. Serum folate levels were negatively correlated with the ages of the pregnant women, and for lactating women, serum folate was positively correlated with their body weights.
The purpose of this study were to determine the folate status of pregnant women living in kwangju, Korea and to assess the relationships between folate status and pregnancy outcome. Eighty-one women took part in the study: 26 in their first trimester of pregnancy, 23 in the second, and 32 in the final trimester. The folate intake data both from their diets and supplementasage was obtained using a 24-hour recall method and by measuring the use of supplements. Folate levels of serum and erythrocytes were determined by a microbiological assay using Lactovacillus casei(ATTC 7469) as the test organism. A series of determinations for pregnancy outcome was conducted, including birth weight, length, Apgar score at 5 min after birth, and gestational period. The dietary folate intake in each trimester was 118$\pm$85, 148$\pm$117, and 137$\pm$69ug/d, respectively. All levels were far below the Korean recommended diet allowances(RDA)for folate. Eighty-four percent of the subjects consumed supplemental folate after the 20th week of pregnancy until delivery. the supplemental folate intakes in the second and third trimester were 651$\pm$142 and 688$\pm$150ug/d, respectively. Therefore, the women who took folate supplements consumed more folate than the RDA. Serum folate levels for each trimester were 9.0$\pm$3.8, 11.4$\pm$6.0, and 16.3$\pm$11.0ng/ml respectively, greadually increasing as the pregnancy progressed; the serum folate level in the third trimester was significantly higher(p<0.05) than that in first trimester. The erythrocyte folate concentrations in each trimester were recorded as 369.8$\pm$108.8, 396.2$\pm$107.5, and 420$\pm$7 162.6ng/ml respectively. There was no significant differences among the erythrocyte folate concentrations unlike the serum folate levels. There was no significant difference among the erythrocyte folate concentrations unlike the serum folate levels. There was no signifcant correlation between trimester to be important in maintaining adequate folate status, however these results imply that the serum and erythrocyte folate levels were adequate to support the growth of the fetus.
It should be concerned to the women with mutated genotype of methylenetetrahydrofolate reductase (MTHFR), C677T or A1298C, since they need more folate than those with wild genotypes. In this study, we evaluated the folate status of Korean women of childbearing age according to their MTHFR polymorpiysm. Dietary folate intakes, plasma and erythrocyte folate concentrations, plasma homocysteine concentrations, and urinary excretions of para-aminobenzoylglutamate (pABG) and para-acetoamidobenzoylglutamate (ApABG) of twenty-five subjects aged between 19 and 35 years old were determined Folate intakes seemed to be inadequate, being only three-quarters of the Korean RDA of folate. More than one-quarter of the subjects was exposed to folate deficiency risk as determined by erythrocyte folate concentration and almost one-quarter of the subjects showed hyperhomocysteinemia, although they had normal plasma folate concentrations. Urinary excretions of pABG and ApABG seemed to be low and ApABG constituted more than $85\%$ of total folate catabolites. There were no significant differences in dietary folate intakes, plasma concentrations of folate and homocysteine, and urinary excretions of pABG and ApABG among the geneotypes of both C677T and A1298C. However, the subjects with 1298AC genotype had significantly lower erythrocyte folate concentration than those with 1298AA. Erythrocyte folate concentration showed an inverse relationship with plasma homocysteine concentration and positive relationships with urinary excretions of pABG and ApABG. The results of this study imply that mutations of 677C$\rightarrow$T and 1298A$\rightarrow$C in the study were not associated with decreased plasma folate and raised plasma homocysteine concentrations. A1298C polymorphism night be, however, more influential on erythrocyte folate concentration than C677T polymorphism, and urinary excretions of folate catabolites, pABG and ApABG, might be reliable indexes of folate nutritional status like plasma homocysteine concentrations.
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