pectins and Vitamin-B-12-Deficiency

Addition of the fermentable fiber pectin to a B12-deficient diet accelerates development of deficiency symptoms. This appears to be the result of changes in the intestinal bacteria that bind vitamin B12, interfere with enterohepatic circulation, and accelerate depletion of this vitamin.

Topics: Animals; Dietary Fiber; Enterobacteriaceae; Fermentation; Pectins; Vitamin B 12; Vitamin B 12 Deficiency

This study examines the effect of dietary fiber supplements of different degrees of bacterial fermentability on biochemical indicators of vitamin B-12 deficiency in rats. Groups of rats were fed a fiber-free diet deficient in vitamin B-12 or the fiber-free diet diluted with 5% of a poorly fermentable dietary fiber (cellulose, lignin or alginic acid) or a highly fermentable fiber (pectin, guar gum or xylan). Poorly fermentable fibers had no significant effect on apparent B-12 status, whereas the highly fermentable fibers significantly increased urinary methylmalonic acid and depressed oxidation of [14C]propionate to 14CO2. Pectin consistently induced significantly greater effects than did xylan or guar gum. The data are consistent with the hypothesis that fermentable fibers stimulate bacterial propionate production and exaggerate certain biochemical indicators of B-12 deficiency. Since pectin had a more pronounced effect than did other fermentable fibers, the possibility that pectin may also interfere with B-12 absorption requires further study.

Topics: Animals; Body Weight; Cellulose; Dietary Fiber; Fermentation; Intestines; Male; Malonates; Methylmalonic Acid; Oxidation-Reduction; Pectins; Propionates; Rats; Rats, Inbred F344; Vitamin B 12 Deficiency

In the present study, rats were depleted of vitamin B-12 with fiber-free or 5% pectin diets, with or without neomycin. Through use of this intestinal antibiotic reported to "spare" vitamin B-12, we sought to determine if bacterial fermentation of pectin might explain our previous observations of negative effects of pectin on vitamin B-12 status. However, neomycin did not lessen interference by pectin with vitamin B-12 metabolism. Pectin increased urinary methylmalonate and decreased propionate oxidation to a greater extent in the presence than in the absence of neomycin. Also, regardless of the presence of neomycin, the biologic half-life of injected [57Co]vitamin B-12 was 58 d for rats fed the fiber-free diets and only 38 d for rats fed 5% pectin diets. Neomycin delayed early fecal excretion of 57Co but had no persistent effect. Thus, neomycin-sensitive bacteria do not mediate the negative effects of pectin on vitamin B-12 status. Pectin may interfere directly with vitamin B-12 absorption or may stimulate vitamin B-12 uptake or propionate production by microbial species that have adapted to neomycin.

Topics: Animals; Diet; Dietary Fiber; Fermentation; Intestinal Absorption; Intestines; Male; Methylmalonic Acid; Neomycin; Nutritional Status; Oxidation-Reduction; Pectins; Rats; Rats, Inbred F344; Vitamin B 12; Vitamin B 12 Deficiency

The effects of thiouracil in correcting defects in folic acid function produced by B12 deficiency were studied. Addition of the thyroid inhibitor, thiouracil, to a low methionine diet containing B12, increased the oxidation of [2-14C]histidine to carbon dioxide, and increased liver folate levels. Addition of 10% pectin to the diet accentuated B12 deficiency as evidenced by a greatly decreased rate of histidine oxidation (0.19%) and an increased excretion of methylmalonic acid. Addition of thiouracil to the diet restored folate function as measured by increased histidine oxidation and increased liver folate levels similar to that produced by addition of methionine to a B12-deficient diet. Thiouracil decreased methylmalonate excretion, and increased hepatic levels of B12 in animals on both B12-deficient and -supplemented diets. Hepatic methionine synthase was increased by thiouracil, which may be the result of the elevated B12 levels. S-Adenosylmethionine and the enzyme methionine adenosyltransferase were also increased by thiouracil. Thus it is possible that the effect of thiouracil in increasing folate function consists both in the effect of thiouracil in decreasing levels of methylenetetrahydrofolate reductase, and also in its action in increasing S-adenosylmethionine which exerts a feedback inhibition of this enzyme.

Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Animals; Carbon Dioxide; Diet; Folic Acid; Histidine; Liver; Male; Methylmalonic Acid; Oxidation-Reduction; Pectins; Rats; Rats, Inbred Strains; Thiouracil; Vitamin B 12; Vitamin B 12 Deficiency

The effect of administering high levels of folic acid to vitamin B12-deficient animals was studied. In B12 deficiency histidine oxidation is decreased. This is the result of both decreased liver folate levels and increases in the proportion of methyltetrahydrofolates. The purpose of this study was to determine if the addition of very high levels of folic acid to B12-deficient diets could increase liver folates and thereby restore histidine oxidation. Rats were fed a soy protein B12-deficient diet containing 10% pectin which has been shown previously to accelerate B12 depletion. When this diet was supplemented with B12 and folic acid, histidine oxidation was 5.4% in 2 h and the livers contained 3.49 micrograms of folate/g. In the absence of B12, the histidine oxidation rate was 0.34% and the liver folate level was 1.33 micrograms/g. When 200 mg/kg of folic acid was added to the B12-deficient diet there was no increase in histidine oxidation (0.35%) but the liver folates were increased to 3.68 micrograms which is about the same as that with B12 supplementation. The percentage tetrahydrofolate of the total liver folates was the same with and without a high level of dietary folic acid. Thus there was an increase in the absolute level of tetrahydrofolate without any increase in folate function as measured by histidine oxidation. Red cell folate levels were the same with and without B12, which is in contrast to the markedly lower liver folate levels in B12 deficiency. These data suggest a difference between B12 regulation of folate metabolism in the liver and in the bone marrow.

Topics: Animals; Body Weight; Diet; Dose-Response Relationship, Drug; Erythrocytes; Folic Acid; Histidine; Liver; Male; Malonates; Pectins; Rats; Rats, Inbred Strains; Tetrahydrofolates; Vitamin B 12 Deficiency

Topics: Animals; Body Weight; Cellulose; Dietary Fiber; Feces; Intestinal Absorption; Methylmalonic Acid; Pectins; Rats; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Animals; Cellulose; Dietary Fiber; Feces; Male; Malonates; Methylmalonic Acid; Pectins; Rats; Vitamin B 12; Vitamin B 12 Deficiency