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Results for “FOLIC ACID DEFICIENCY”

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PubMed2002

Plasma, liver and kidney folate and plasma homocysteine concentrations are poor response variables at very low dietary folate intakes, in a folate depletion/repletion rat model.

Folate depletion/repletion rat models are popular protocols for assessing the bioavailability of folate. Much of the early work carried out on folate bioavailability concentrated on foods naturally high in folate. However, foods low in folate often contribute significantly to folate intake because of their high consumption in the general population. Therefore, the assessment of the bioavailability of foods low in folate is essential to properly estimate folate intake. The present study investigated plasma, liver and kidney folate and plasma homocysteine concentrations as appropriate response variables for measuring folate bioavailability in the rat at very low dietary folate intakes. One hundred and one weanling male rats (Wistar strain) were fed a folate-deficient diet containing 1% succinyl sulfathiazole for 28 d. Following depletion, six rats were randomly assigned to each of 16 repletion diets containing folic acid, fortified white bread, unfortified wholemeal bread or unfortified rye bread calculated to provide 6.25, 12.5, 18.75 and 25 micrograms folate/kg of each diet. After a further 28 d, plasma, liver and kidney folate concentrations were determined by microbiological assay. Plasma homocysteine was measured by HPLC as a functional indicator of folate status. Only a weak correlation was found between the response variables measured and dietary folate intake, indicating that this folate depletion/repletion rat model is not suitable for testing the response of rats fed diets containing very low levels of folate.

Animals↗
PubMed1991

Folate deficiency and an abnormal lymphocyte deoxyuridine suppression test in monkeys.

Cebus albifrons were fed folate-deficient diets in order to assess folate status at the cellular level with the deoxyuridine suppression test. Plasma and red blood cell folates were significantly lower at 2 months, compared to control values. Hematologic signs of megaloblastic anemia occurred after 6 months, with significantly lower hematocrit, hemoglobin and red blood cell number values and increased polymorphonuclear leukocyte lobe counts. Urinary formiminoglutamic acid excretion also was elevated significantly. Whole blood lymphocyte cultures exhibited abnormal deoxyuridine suppression of [3H]-thymidine incorporation into DNA with folate deficiency. Thus this deoxyuridine suppression test can be used in isolated whole blood lymphocytes of these nonhuman primates to document folate deficiency.

Animals↗
PubMed1962

Absorption of folic acid from the small intestine of the rat.

The absorption of folic acid from segments of the small intestine of the rat has been measured in situ with tritium-labelled folic acid. The fraction absorbed was independent of concentration below 10(-6) M but was depressed to half at 4x10(-5) M. Direct measurements of fluxes showed that the mucosal --> serosal flux was about 14 times the serosal --> mucosal flux, and therefore that uptake of folic acid is an active process. In the ileum but not in the duodeno-jejunum, absorption was depressed by the presence of electrolyte. There was little difference in absorptive capacity between jejunum and ileum nor was there any significant change in animals suffering from a dietary deficiency of folic acid.

Animals↗
PubMed1995

DNA damage in folate deficiency.

Folate deficiency significantly increases uracil content and chromosome breaks (as measured by micronucleated cells) in human leukocyte DNA. Folate supplementation reduces both the uracil content of DNA and the frequency of micronucleated cells, indicating that uracil misincorporation may play a causative role in folate deficiency-induced chromosome breaks. A calculation is presented to explain how the levels of uracil found in DNA could cause chromosome breaks. Based on this calculation, the frequency of uracil repair events that might result in double-strand DNA breaks increases by 1752-fold. These results are consistent with clinical and epidemiological evidence linking folate deficiency to DNA damage and cancer.

DNA Damage↗
PubMed1991

Folate deficiency and pregnancy outcome.

The degree of folate deficiency can be manipulated in rats by the extent of exposure to a deficient diet. In turn, this can affect pregnancy outcome and neonatal health.

Animals↗
PubMed1975

Folates and the fetus.

Folate metabolism is sometimes deranged in the early weeks of pregnancy at the time of placentation and organogenesis. Maternal folate deficiency may result in general impairment of fetal growth, which is reflected in low birthweight. Such women also have a high incidence of abortion, abruptio placentae and fetal malformation. Megaloblastic anaemia is the commonest and most easily recognised manifestation of folate deficiency.

Abortion, Spontaneous↗
PubMed1989

[Folate and vitamin B12 deficiency. Characterization of parameters for early diagnosis].

True vitamin B12/folate deficiency is more common than is currently appreciated; it appears in many guises and the classic hematological features of megaloblastic anaemia are often absent. The single most reliable predictor of megaloblastic anaemia is serum vitamin B12/folate concentration, but this determination in a screening program for all patients is difficult in terms of laboratory overload and cost. Early recognition of nutritional anaemias is, however, mandatory and we undertook this study to explore the possibility of identifying, on a demographic basis or because of routine laboratory results, a group of subjects at risk for vitamin B12/folate deficiency. Results obtained in simultaneous radioassay of serum B12 and folate levels and erythrocyte folate concentration in 1.200 hospitalized patients are presented. Coexisting iron deficiency was excluded by ferritin assay. We found no significant difference between males and females and no correlation between serum folate and B12 concentrations and aging. Low serum folic and cobalamin levels were found in 53% of patients with macrocytosis and elevated MCH, even in the absence of anaemia. These observations suggest that increased MCV and MCH may be present before a related anaemia and that serum folate and cobalamin levels must be monitored early in these patients to prevent a deficiency.

Age Factors↗
PubMed1985

[Evaluation of the folacin status in children with regard to the cobalamin and iron status. 1. Changes in the differential blood picture as a function of the vitamin and ferritin levels of the serum vs. erythrocytes].

The biochemical data concerning the evaluation of the folacin status in children are insufficient, as there are no biologically based borderlines available. In a study with 165 children between 1 and 15 years we looked for serum and erythrocytic folate concentrations and correlated the results with morphological alterations in the blood picture (lobe average of the neutrophilic granulocytes). As cobalamin and iron status influences different folacin depending parameters we estimated the vitamin B12- and ferritin concentration in serum as well. In our study neither the iron nor the cobalamin status influenced the blood picture and the blood folate concentrations. That's why all samples could be taken for the final evaluation. It could be demonstrated that folacin serum levels below 4.0 ng/ml respectively erythrocytic concentrations below 250 ng/ml correspond with an increasing lobe average above 3.5 compared with normal values ranging between 2.8-3.5. These biologically based borderlines were comparable between the different age groups. On the basis of these data it is possible to assess the duration and severity of folacin deficiency in children.

Adolescent↗
PubMed1981

Effect of folate deficiency on the digestive and absorptive functions of intestinal epithelium in rats.

The effect of folate deficiency, induced by a folate deficient diet, on the digestive and absorptive functions of the intestinal epithelium in rats has been investigated. The intestinal uptake of D-glucose and L-alanine and the brush border sucrase, lactase and alkaline phosphatase activities were considerably depressed in folate deficient animals compared to the control group. Kinetic studies with brush border sucrase in control and deficient animals revealed that reduced levels of the enzyme in folate deficiency are due to a reduced number of enzyme molecules. There was no change in activity of lactate-dehydrogenase in enterocytes of folate deficient rats.

Alanine↗