Pyridoxine-deficient Diet Research Articles

Vitamin B12 Optic Neuropathy in Autism

Dietary vitamin B12 deficiency was identified as a cause of partially reversible optic neuropathy in 3 autistic children. All of the affected children presented with gradual visual loss. Examination revealed optic atrophy, and further questioning regarding diet revealed that all 3 children had severe food selectivity and highly stereotyped diets that resulted in an almost total lack of animal products in their diets. Vitamin B12 levels were low in all 3 children. Treatment with intramuscular vitamin B12 and normalization of vitamin B12 levels resulted in improvement of visual functioning in all 3 children. These cases illustrate that food selectivity, a known complication of autism, can result in vitamin deficiency that can cause visual loss and optic atrophy. Physicians must have a high index of suspicion when evaluating children with autism and visual loss to detect this rare cause of optic atrophy.

Developmental retardation due to dietary vitamin B12 deficiency during infancy

History: We report on a seven-month-old infant presenting with developmental retardation of unclear origin. After an uneventful pregnancy and birth he first reached his developmental milestones in time. At the age of four months his development came to a halt and he failed to thrive. Furthermore, he had muscular hypotonus and suffered from dysphagia and apathy. Till then he was completely breast-fed. The patient is the first child of non-consanguine parents. The parents did not suffer from any relevant disorders. Results: The cranial MRI showed normal myelination, but atrophy of the brain. His EEG revealed minor general alterations. The results of eye examination and audiometry were normal. Primary blood examination uncovered megaloblastic anemia and hyperhomocysteinemia. Urinary analysis of organic acids showed increased levels of methylmalonic acid, while the serum levels of methionine were low. A vitamin B12 deficiency was found to be the reason for these changes. Blood samples of the mother also showed low levels of vitamin B12. Therapeutic measures: Vitamin B12 was substituted by intramuscular cobalamin injections in a dosage of 1mg over 2 days. Nutrition was changed from breast-feeding to formula. Already three weeks later, his laboratory results were normal except for a minor elevation of the homocystein serum levels. Apathy and dysphagia dissolved and there was progress in his motor development. Discussion: Decreased levels of vitamin B12 during infancy are usually found in breast-fed infants due to a lack of vitamin B12 in breast milk, particularly when mothers are vegans or suffer from pernicious anemia. In contrast, vitamin B12 deficiency due to congenital metabolic disorders is very rare. By substitution one can reach a partial normalisation of symptoms, but early recognition of the deficiency is crucial. Even with successful substitution, long term consequences such as substandard intellectual capacities may persist.

Antioxidative status and lipid peroxidation in kidney tissue of rats fed with vitamin B6-deficient diet

Introduction: The aim of this study was to evaluate lipid peroxidation (LP) and free radical scavenging enzyme activities in kidney tissue of vitamin B6-deficient rats. Material and Methods: The rats were divided into control and vitamin B6-deficient groups. After 4 weeks of feeding, animals in all groups were anesthetized by thiopental sodium (50 mg/kg). Thoraces were opened, 2 mL blood samples were taken from aortas, then the rats were killed by cervical dislocation, and kidney tissues were removed. Biochemical measurements in kidney tissue were carried out using a spectrophotometer. Results: Total superoxide scavenger activity (TSSA), nonenzymatic superoxide scavenger activity (NSSA), superoxide dismutase (SOD) activities, and antioxidant potential (AOP) values in the vitamin B6-deficient group were significantly lower than those of the control group, whereas glutathione peroxidase (GSH-Px), glutathione reductase (GRD), glutathione-S-transferase (GST) activities, and malondialdehyde (MDA) level were significantly higher than those of the control group (p < 0.05). Discussion: The results show that vitamin B6 deficiency causes an attenuation in antioxidant defense system and an increase in oxidative stress in kidney tissue of rats.

Deficiencies of folate and vitamin B12 do not affect fracture healing in mice

Purpose Recently, hyperhomocysteinemia has been shown to be associated with impaired fracture healing in mice. The main causes for hyperhomocysteinemia are deficiencies of folate and vitamin B12. However, there is no information on whether deficiencies of these B vitamins are affecting bone repair, too. Methods We used two groups of mice to investigate the impact of folate and vitamin B12 deficiency on fracture healing: mice of the first group were fed a folate- and vitamin B12-deficient diet ( n = 14), while mice of the second group received an equicaloric control diet ( n = 13). Four weeks after stabilizing a closed femur fracture, bone repair was analyzed by histomorphometry and biomechanical testing. In addition, serum concentrations of homocysteine, folate, vitamin B12, the bone formation marker osteocalcin (OC), and the bone resorption marker collagen I C-terminal crosslaps (CTX) were measured. Results Serum analyses revealed significantly decreased concentrations of folate and vitamin B12 in animals fed the folate- and vitamin B12-deficient diet when compared to controls. This was associated with a moderate hyperhomocysteinemia in folate- and vitamin B12-deficient mice, while no hyperhomocysteinemia was found in controls. Three-point bending tests showed no significant differences in callus stiffness between bones of folate- and vitamin B12-deficient animals and those of control animals. In accordance, the histomorphometric analysis demonstrated a comparable size and tissue composition of the callus, and also serum markers of bone turnover did not differ significantly between the two groups. Conclusions We conclude that folate and vitamin B12 deficiency does not affect bone repair in mice.

Taurine-deficient diet up-regulated cystathionine β-synthase monoallele in hemizygous cystathionine β-synthase knockout mice

Impaired cystathionine beta-synthase (CBS) causes hyperhomocystinuria and hyperhomocysteinemia, both risk factors for cardiovascular diseases. Reduced CBS activity could decrease cysteine and taurine biosyntheses (metabolites of homocysteine degradation) and lead to less taurocholic acid production with a resultant increased cholesterol content. We hypothesized that a deficiency in CBS genetic material and enzyme activity would reduce taurine synthesis, which would lead to an elevated cholesterol concentration. Both sexes of hemizygous C57BL/6J-Cbs(tm1Unc) [CBS (+/-)] and wild-type C57BL/6J mice [CBS (+/+)] were divided into 2 groups. One group of CBS (+/-) and CBS (+/+) mice was fed a cysteine- and taurine-deficient diet for 8 weeks, and the other group was fed a cysteine, taurine, and vitamin B6-deficient diet for 8 weeks. Significantly higher plasma total homocysteine concentrations occurred in the CBS (+/-) mice than their CBS (+/+) cohorts. Female mice of both genotypes had significantly higher plasma total homocysteine concentrations and significantly lower relative CBS mRNA levels than did male mice. During vitamin B(6) deficiency, plasma total homocysteine concentrations were significantly elevated. Three important findings were a differential sex response of CBS mRNA to feeding the vitamin B(6) diet; CBS (+/-) mice had a significantly lower plasma cholesterol concentration, contrary to what was anticipated; and during feeding, the taurine- and cysteine-deficient diet, CBS mRNA levels in CBS (+/-) mice were reduced only 13% rather than the expected 50%. We conclude that the remaining CBS monoallele is up-regulated in mice when fed a taurine-deficient diet to produce additional CBS mRNA.

The effects of pyridoxine deficiency and supplementation on hematological profiles, lymphocyte function, and hepatic cytochrome P450 in B6C3F1 mice

Pyridoxine, a B6 vitamin, is a co-factor in a variety of enzymatic reactions involved in intermediary metabolism. The effects of pyridoxine deficiency and supplementation on hematological profiles, lymphocyte function, and hepatic CYP1A1 and CYP2E1 were investigated in B6C3F1 mice fed a diet containing either 0 (i.e., pyridoxine-deficient diet, [PD]); or 7 mg pyridoxine-HCl/kg (i.e., control diet, [CD]) for 8 or 13 weeks followed by administration of 500 μg pyridoxine-HCl (IP) daily for either 2 (PD-S2 and CD-S2) or 3 (PD-S3 and CD-S3) consecutive days. Results demonstrated that erythrocyte aspartate aminotransferase activity coefficient (EAST-AC) values, which reflect host pyridoxine status, were significantly higher in PD mice than in CD mice, and dropped to control levels after supplementation. PD mice had significantly reduced weight gains, mean corpuscular volume (MCV), hemoglobin (HGB), and hematocrit (HCT) levels compared to CD mice after 8 and 13 weeks on the prescribed diet. In addition, PD mice had significantly lower circulating levels of total white blood cells, but higher red blood cell numbers after 8 weeks (compared to CD mice). Pyridoxine supplementation for 3 days restored HGB levels in PD mice to that of the unsupplemented CD controls; HCT, MCV and MCH levels were also increased in PD-S3 mice compared to their unsupplemented PD counterparts, but failed to reach comparable levels to those seen in mice fed a control diet. The pyridoxine-deficient diet also resulted in decreased mitogen stimulated T-lymphocyte proliferation after a 13-week feeding regimen and increased hepatic CYP1A1 activity that was reversed by pyridoxine supplementation. These studies demonstrate in a murine model that pyridoxine deficiency can cause multiple alterations that, in many cases, can be reversed by supplementation.

Serum homocysteine in Indian adolescents

To assess serum homocysteine levels and its association with conventional risk factors for cardiovascular disease (CVD) in Indian adolescents. This was a cross-sectional study conducted in tertiary care hospital in northern India in apparently healthy adolescents aged 10-19 yr. A pre-designed questionnaire was used to assess conventional risk factors. Serum homocysteine levels of > or = 12 micromol/L, serum triglycerides > or = 150 mg% and serum cholesterol > or = 200 mg% were taken as hyperhomocysteinemia, hypertriglyceridemia and hypercholesterolemia, respectively. Serum high-density lipoprotein (HDL) > or = 40 mg% was considered protective for CVD. In 103 subjects, 36.87 % females, mean serum homocysteine level was 11.649 +/-0.416 micromol/L. Hyperhomocysteinemia was present in 46 (44.6%, 95% CI: 34.965-54.75) subjects. Dietary deficiency of vitamin B12 and folic acid, body mass index (BMI) > 84(th) percentile and altered lipid profile were associated with hyperhomocysteinemia on univariate analysis. After multivariate adjustment for BMI and vegetarian diet, low serum HDL (OR: 23.81, 95% CI: 2.86-200; p = 0.003) and serum hypertriglyceridemia (OR: 4.17, 95% CI: 1.51-13.51; p = 0.022) had independent association with hyperhomocysteinemia. Since we have also found an association between hyperhomocysteinemia and low serum HDL levels and hypertriglyceridemia, which are conventional risk factors for CVD, interventional strategies are urgently needed among adolescents for prevention of CVD.

Maternal MTHFR 677C>T genotype and dietary intake of folate and vitamin B12: their impact on child neurodevelopment

Using the Bayley test, the mental and psychomotor development in a cohort of 253 children were evaluated. Maternal dietary intake of vitamin B12 and folate was assessed from a semiquantitative questionnaire administered during the first trimester of pregnancy. Maternal genotypes of MTHFR (677C>T and 1298A>C), were ascertained by PCR-RFLP. The 677T and 1298C variant alleles were present in 59% and 10% of participants, respectively. A dietary deficiency of vitamin B12 was negatively associated with mental development (β = −1.6; 95% CI = −2.8 to −0.3). In contrast, dietary intake of folate (< 400 mg/day) reduced the mental development index only among children of mothers who were carriers of the TT genotype (β = −1.8; 95% CI = −3.6 to −0.04; P for interaction = 0.07). Vitamin B12 and folate supplementation during pregnancy could have a favorable impact on the mental development of children during their first year of life, mainly in populations that are genetically susceptible.

Impairments in pyridoxine-dependent sulphur amino acid metabolism are highly sensitive to the degree of vitamin B6 deficiency and repletion in the pig

The objectives of the current study included the characterization of the temporal changes in indices of sulphur amino acid metabolism in piglets in response to vitamin B6 deficiency and repletion with graded levels of pyridoxine hydrochloride. In Experiment 1, 12 piglets (average initial weight = 5.3 kg; n = 6 per group) were fed a semi-purified diet containing either 0 (deficiency group) or 3 mg (control group) pyridoxine·HCl/kg diet, using a pair-feeding design, for 6 weeks. Piglets consuming vitamin B6-deficient diets exhibited decreased average daily gains on the 4th week and feed conversion efficiency from the 4th week until the end of the trial (P < 0.05). Plasma pyridoxal-5′-phosphate (PLP), in pigs consuming vitamin B6-deficient diets, was significantly lower than controls throughout the experiment (P < 0.01), reaching a nadir of 14% of the control animals’ value by the end of the trial. Indices of sulphur amino acid metabolism, including activities of hepatic cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CGL) and serine hydroxymethyltransferase, as well as hepatic-free cysteine concentrations were markedly decreased after 6 weeks of B6 deficiency (P < 0.05). Total hepatic mRNA expressions for CBS and CGL were not affected. Concurrently, hepatic-free homocysteine concentrations increased by more than eight-fold (P < 0.01) at the end of the trial. An examination of plasma total homocysteine and cysteine concentrations revealed significant (P < 0.05) differences between treatments, with evidence of an abrupt shift in concentrations at 3 weeks post-initiation of dietary treatments (>25-fold increase in homocysteine; halving of cysteine values). At the end of Experiment 1, vitamin B6 deficiency significantly increased plasma methionine and serine levels, but decreased plasma glycine concentrations (P < 0.05). In Experiment 2, 20 pigs of 14 days old (initial BW = 5.0 kg) were subjected to a 4-week vitamin B6 depletion protocol, based on results obtained in Experiment 1. After the depletion period and assessment of baseline status (four pigs), remaining pigs were allocated to one of four dietary vitamin B6 repletion treatments: 0.75, 1.5, 2.25 and 3 mg/kg diet as pyridoxine·HCl (n = 4 per level) for 14 days. Significant dose-dependent increases in plasma PLP and cysteine, and decreases in homocysteine were observed, and these were sensitive to the duration of repletion. In conclusion, data from the current studies support the use of both plasma PLP and homocysteine as sensitive indices of vitamin B6 status in the pig. Additionally, the observed patterns of responses in vitamin B6-sensitive metabolites are supportive of an inclusion level of 2.25 mg/kg diet, as pyridoxine·HCl, in diets for young pigs.

Endogenous oxalogenesis after acute intravenous loading with ethylene glycol or glycine in rats receiving standard and vitamin B6‐deficient diets

The effect on endogenous oxalate synthesis of acute intravenous loading with ethylene glycol or glycine was investigated in rats on a standard or a vitamin B6-deficient diet. Twenty-four male Wistar rats weighing approximately 180 g were randomly divided into ethylene glycol and glycine groups of 12 animals each. These groups were further divided into two subgroups of six animals each that were fed either a standard or a vitamin B6-deficient diet for 3 weeks. Animals of these two subgroups received an intravenous infusion of 20 mg (322.22 micromol) of ethylene glycol or 100 mg (1332.09 micromol) of glycine, respectively. Urine samples were collected just before intravenous infusion of each substance and at hourly intervals until 5 h after receiving the infusion. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. Urinary oxalate and glycolate excretion was significantly increased after ethylene glycol administration. Significant differences between the control and vitamin B6-deficient groups were found. In contrast, there were only small changes of oxalate and glycolate excretion after glycine administration. Recovery of the given dose of ethylene glycol as oxalate in 5-h urine was 0.31% and 7.15% in the control and vitamin B6-deficient groups, respectively, whereas recovery of glycolate was 0.68% and 7.22%, respectively. Ethylene glycol loading has a significant effect on urinary oxalate excretion in both normal and vitamin B6-deficient rats, whereas glycine loading only has a small effect. Oxalate and glycolate excretion after ethylene glycol loading were respectively 23-fold and 11-fold higher in vitamin B6-deficient rats than in controls.

Immunosuppressive effects of 2-acetyl-4-tetrahydroxybutyl imidazole (THI) in the rat

THI is a component of ammonia caramel, a widely used food colouring. The effect of THI on the immune system has been determined in the male F344 rat. THI was given in the drinking water at doses of 1, 10 and 50 mg/l (equivalent to 0.1, 1 and 5 mg/kg per day) to animals on a vitamin B6-deficient diet. After 1 week, the immune competence of the animals was assessed under continued THI treatment. No marked changes in thymus or spleen weight were observed after THI treatment, although there was an increased number of pyknotic cells in the thymic cortex, mainly engulfed by macrophages and there appeared to be a slight thinning of the cortex area. THI produced a significant loss in T and B lymphocytes in peripheral blood but not in the spleen. No change in natural killer (NK) cell activity against YAC-1 target cells was observed in the spleen. The observed increase in NK cell activity in peripheral blood was due to an increase in circulating large granular lymphocytes (LGL). Although the serum antibody titre against keyhole limpet haemocyanin (KLH) was not affected by THI treatment, B cells showed less proliferation when cultured with lipopolysaccharide. T cell function was impeded as measured in mitogen-induced proliferation assay, delayed-type hypersensitivity assay and host versus graft (popliteal lymph node) assay. The results indicate that THI is an immunosuppressor in the rat, in whom it can produce profound lymphopenia and suppression of cell-mediated immunity.

Effects of maternal vitamin B12 deficiency from end of gestation to weaning on the growth and haematological and immunological parameters in mouse dams and offspring

Vitamin B12-deficiency may induce specific symptoms as neurological alterations and unspecific symptoms such as anaemia and growth retardation. In this study, maternal vitamin B12 deficiency from end of gestation to weaning was evaluated in mouse dams, which was provoked by feeding a vitamin B12-deficient diet. The animals were divided into two groups (control and deficient). The control group received the vitamin B12-deficient diet supplemented with commercial vitamin B12. Compared to the control, the vitamin B12-deficient dams and their offspring showed a significant decrease of body weight (by 20 and 39%, respectively), serum vitamin B12 concentration (by 61 and 67%, respectively), haematological values as haematocrit (25 and 26%, respectively), and IgA producer cells (by 36 and 54%, respectively). In both, vitamin B12-deficient mouse dams and their offspring, histological alterations of small intestine were observed, whereas growth retardation occurred in the offspring only. This experimental murine model allows assessing the incidence of maternal cobalamin deficiency in offspring and would be useful for evaluating novel adjuncts such as functional foods to prevent vitamin B12 deficiency.

Vitamin B12deficiency results in the abnormal regulation of serine dehydratase and tyrosine aminotransferase activities correlated with impairment of the adenylyl cyclase system in rat liver

The aim of the present study was to elucidate the mechanism of the vitamin B(12) deficiency-induced changes of the serine dehydratase (SDH) and tyrosine aminotransferase (TAT) activities in the rat liver. When rats were maintained on a vitamin B(12)-deficient diet, the activities of these two enzymes in the liver were significantly reduced compared with those in the B12-sufficient control rats (SDH 2.8 (sd 0.56) v. 17.5 (sd 6.22) nmol/mg protein per min (n 5); P < 0.05) (TAT 25.2 (sd 5.22) v. 41.3 (sd 8.11) nmol/mg protein per min (n 5); P < 0.05). In the B(12)-deficient rats, the level of SDH induction in response to the administration of glucagon and dexamethasone was significantly lower than in the B(12)-sufficient controls. Dexamethasone induced a significant increase in TAT activity in the primary culture of the hepatocytes prepared from the deficient rats, as well as in the cells from the control rats. However, a further increase in TAT activity was not observed in the hepatocytes from the deficient rats, in contrast to the cells from the controls, when glucagon was added simultaneously with dexamethasone. The glucagon-stimulated production of cAMP was significantly reduced in the hepatocytes from the deficient rats relative to the cells from the control rats. Furthermore, the glucagon-stimulated adenylyl cyclase activity in the liver was significantly lower in the deficient rats than in the controls. These results suggest that vitamin B(12) deficiency results in decreases in SDH and TAT activities correlated with the impairment of the glucagon signal transduction through the activation of the adenylyl cyclase system in the liver.

Vitamin B6 Deficiency can Reduce Fuel Storage and Utilization in Physically Trained Rats

This study investigated the effect of vitamin B6 deficiency on the utilization and recuperation of stored fuel in physically trained rats. 48 rats were given either vitamin B6-deficient (B6-) diet or control (B6) diet for 4 weeks and were trained on treadmill for 30 minutes daily. All animals were then subdivided into 3 groups: before-exercise (BE); during-exercise (DE); after-exercise (AE). The DE group was exercised on treadmill for 1 hour just before being sacrificed. Animals in the AE group were allowed to take a rest for 2 hours after being exercised like the DE group. Glucose and free fatty acids were compared in plasma. Glycogen and triglyceride were compared in liver and skeletal muscle. Protein levels were compared in plasma, liver, and skeletal muscle. Compared with the B6+ group, plasma glucose levels of the B6- group were significantly lower before and after exercise. Muscle glycogen levels of the B6- group were significantly lower than those of the B6+ group regardless of exercise. The liver glycogen level of the B6- group was also significantly lower than that of B6+ group during and after exercise. Before exercise, plasma free fatty acid levels were not significantly different between the B6+ and B6- groups, and plasma free fatty acid levels of the B6- group were significantly lower during and after exercise. The muscle triglyceride level of the B6- group was significantly lower than that of the B6+ group before exercise, and there were no differences between B6+ and B6- groups during and after exercise. Liver triglyceride levels were not significantly different between B6+ and B6- groups. Plasma protein levels of the B6- group were lower than those of B6+ before and after exercise. Muscle protein levels of the B6- group were not significantly different from those of the B6 group. Liver protein levels of the B6- group were significantly lower than that of the B6+ group after exercise. Liver protein levels of both B6+ and B6- groups were not significantly changed, regardless of exercise. Thus, it is suggested that vitamin B6 deficiency may reduce fuel storage and utilization with exercise in physically trained rats.

Vitamin B6 deficiency augments endogenous oxalogenesis after intravenous l-hydroxyproline loading in rats

The effects of an intravenous hydroxyproline load on endogenous oxalogenesis were compared in rats fed a standard diet or a vitamin B6-deficient diet. Twelve male Wistar rats were randomized to two groups and were fed either a standard diet (control group) or a vitamin B6-deficient diet for 3 weeks. Then the animals were intravenously administered 100 mg (762.6 micromol)/ml hydroxyproline. In the control group, infusion of hydroxyproline increased the 5-h urinary oxalate and glycolate excretion above baseline to 0.27% (2.02 +/- 1.11 micromol) and 0.32% (2.43 +/- 1.60 micromol) of the administered dose (mol/mol), while it was respectively 2.01% (15.24 +/- 2.13 micromol) and 0.00% (-0.02 +/- 0.19 micromol) of the dose in the vitamin B6-deficient group. Therefore, vitamin B6 deficiency augmented endogenous synthesis of oxalate from hydroxyproline by 7.56-fold (15.24/2.02) compared with that in the control group. Urinary citrate excretion was significantly lower at baseline and all other times in the vitamin B6-deficient group compared with the control group. In conclusions, L-hydroxyproline loading augmented endogenous oxalogenesis in the vitamin B6-deficient group without causing hyperglycolic aciduria, and also led to significant hypocitraturia. These findings suggest that hydroxyproline is not metabolized to oxalate via glycolate, but rather via the 4-hydroxyglutamate to glyoxylate pathway (usually requiring vitamin B6-dependent enzymes) even in the presence of vitamin B6 deficiency.

Role of Vitamin B6 Deficiency in the Nitrogen Balance of Streptozotocin-Diabetic Rats

ABSTRACTMale Wistar rats with streptozotocin-induced diabetes received a control diet and a pyridoxine-deficient diet. The animals were divided at random into four groups: control rats (CR), control diabetic rats (CDR), diabetic rats receiving a pyridoxine-free diet (DRB6), and diabetic rats receiving saline solution and no insulin treatment (DRSS). The experiment lasted 45 days. During the first 15 days the animals were observed for the development of diabetes and during the remaining 30 days they received the respective diets. The absence of vitamin B6 did not influence the glycemia levels at the end of the experiment or the weight evolution of the animals. The rats that did not receive pyridoxine (DRB6) only showed a reduction in GPT activity (17.79 U/mL) compared to the other groups. The DRB6 group presented a significantly lower (p <0.05) nitrogen balance during each period (2.38 ± 0.44 g N/7 days) compared to the CDR group (3.28 ± 0.56 g N/7 days). The DRSS group presented similar or significantly higher values (2.81 ± 0.77 g N/7 days) compared to the CDR group. Pyridoxine-deficient diabetic rats treated with insulin suffered important changes in the utilization of dietary proteins, as observed by nitrogen balance and enzyme activity studies.

Testicular Injury to Rats Fed on Soybean Protein-Based Vitamin B12-Deficient Diet Can Be Reduced by Methionine Supplementation

We have previously reported that rats fed on a vitamin B12 (B12)-deficient diet containing 180 g soybean protein per kg diet showed marked histologic damage in their testes. In this paper, we report the effect of B12-deficiency on B12-dependent methionine synthase in the rats' testes and the effect of methionine supplementation of the diet on testicular damage. Rats were fed the soybean protein-based B12-deficient diet for 120 d. We confirmed that those rats were in serious B12-deficiency by measuring urinary methylmalonic acid excretion and B12 content in tissues. Methionine synthase activity in the testis of the B12-deficient rats was less than 2% of that in B12-supplemented (control) rats. To complement disrupted methionine biosynthesis, methionine was supplied in the diet. A supplement of 5 g D,L-methionine per kg diet to the B12-deficient diet did not affect urinary methylmalonic acid excretion of B12-deficient rats. The testicular histology of rats fed the methionine-supplemented B12-deficient diet was almost indistinguishable from that of control rats. Thus, we conclude that the lowered testicular methionine synthase activity is the primary cause of the histologic damage due to B12-deficiency and that methionine supplementation to the diet can reduce the damage. These findings would indicate the importance of the methionine synthase activity, especially for testicular function.

Prenatal Dietary Deficiency of Vitamin B12 and Neurodevelopment During the First Year of Life

Prenatal Dietary Deficiency of Vitamin B12 and Neurodevelopment During the First Year of Life

Prenatal Dietary Deficiency of Vitamin B12 and Neurodevelopment During the First Year of Life

Prenatal Dietary Deficiency of Vitamin B12 and Neurodevelopment During the First Year of Life

Effect of vitamin B6 deficiency on the utilization of fuel with exercise in rats

Forty eight rats were fed either a control diet (+B6) or vitamin B6 deficient diet (-B6) diet for 4 weeks and were subdivided into 3 groups: before exercise (BE); during exercise (DE); after exercise (AE). DE group were exercised on treadmill for 1 hours just before sacrifice at the end of 4th week of respective diet and AE group were recuperated 1 hour after exercised like DE group. The levels of glucose (GLU), glycogen (GLY), protein (PRO), free fatty acid (FFA) and triglyceride (TG) were compared in plasma, liver and skeletal muscle. There were no differences between +B6 and -B6 in muscle and liver GLY before and during exercise but liver GLY was not recovered and 40% lower after exercise in –B6 group. Muscle TG was decreased with exercise in +B6 group(15% in DE, 28% in AE) but was not changed with exercise in –B6 group. Liver TG was decreased with exercise in -B6 group(26% in AE) but was not changed with exercise in +B6 group. Plasma FFA was increased with exercise in +B6 group(18% in DE, 16% in AE) while was decreased with exercise in –B6 group(35% in DE, 38% in AE). There were no changes in plasma, liver and muscle PRO of both +B6 and –B6 group with exercise. These results suggest that vitamin B6 deficiency may influence the utilization of fuel stores.