Accumulation of lipid in rat liver was induced by vitamin B6 deficiency and was ameliorated by supplemental phosphatidylcholine in the diet.

We investigated the efficacy of supplementing the diet with pteroylmonoglutamic acid (PGA), choline, or phosphatidylcholine (PC) in ameliorating the lipid accumulation in rat liver that is induced by vitamin B6 (B6) deficiency. In Experiment 1, male Wistar rats were fed a control, B6-deficient, or PGA-, choline-, or PC-supplemented (10 mg, 4 g, and 6.3 g/kg of diet, respectively) B6-deficient diet containing l-methionine at 9 g/kg of diet for 35 days. In Experiment 2, rats were fed a control, B6-deficient, or PC-supplemented (at 3.15, 6.3, or 12.6 g PC/kg of diet) B6-deficient diet for 35 days. Choline or PC supplementation ameliorated liver lipid deposition and returned plasma lipids to normal. Judging from these results, it appeared that B6 deficiency decreased the synthesis of PC in the liver, thereby decreasing the secretion of very low-density lipoproteins, and in consequence producing lipid accumulation in the liver and reductions of plasma lipids.

Involvement of 5-methyltetrahydrofolate in the amelioration of hyperhomocysteinemia caused by vitamin B(6) deficiency and L-methionine supplementation.

We attempted to clarify the reason why folate fortification ameliorates hyperhomocysteinemia induced by vitamin B(6) deficiency. Hyperhomocysteinemia caused by vitamin B(6) deficiency significantly decreased the rat liver 5-methyltetrahydrofolate level which was significantly improved by folate fortification. This result suggests that the amelioration of hyperhomocysteinemia in response to folate supplementation had enhanced the removal of homocysteine via methionine synthase.

[Does diet affect our mood? The significance of folic acid and homocysteine]. / Czy dieta ma wplyw na nasz nastrój? Znaczenie kwasu foliowego i homocysteiny.

UNLABELLED: In recent years, there has been growing interest in the association between national diet and the possibility of developing various mental disorders, as well as between deficiency of such vitamins as, e.g. folic acid, vitamin B12, B6, and others (e.g., omega-3 fatty acids), elevated serum homocysteine level and the functioning of human brain as well as the occurrence of such disorders as dementia, central nervous system vascular disorders and depression. THE AIM OF THE STUDY: was to present the current state of knowledge about the role of folic acid and homocysteine in the human organism as well as the significance of vitamin deficiency, mainly folic acid and hyperhomocysteinemy for the occurrence of mood disorders. METHOD: The authors conducted the search of the Internet database Medline (www.pubmed.com) using as key words: depression, mood, homocysteine, vitamin deficiencies: folic acid, B6 and 812 and time descriptors: 1990-2007. RESULTS: In depression, folate, vitamins B12 and B6, as well as unsaturated omega-3 fatty acids deficiency affects the biochemical processes in the CNS, as folic acid and vitamin B12, participate in the metabolism of S-adenosylmethionine (SAM), a donator of methyl groups, which play a decisive role in the functioning of the nervous system; they are, among others, active in the formation of neurotransmitters (e.g. serotonin), phospholipids that are a component of neuronal myelin sheaths, and cell receptors. The deficiency of the vitamins in question results in hyperhomocysteinemia (the research shows that approximately 45-55% of patients with depression develop significantly elevated serum homocysteine), which causes a decrease in SAM, followed by impaired methylation and, consequently, impaired metabolism of neurotransmitters, phospholipids, myelin, and receptors. Hyperhomocysteinemia also leads to activation of NMDA receptors, lesions in vascular endothelium, and oxidative stress. All this effects neurotoxicity and promotes the development of various disorders, including depression. Vitamins B12 and B6, folic acid and omega-3 fatty acids supplementation is thus important in patients suffering from their deficiency; national diet as a significant factor in prevention of numerous CNS disorders, including depression, is also worth consideration.

Estudio de las repercusiones clínicas y analíticas de una intervención nutricional en pacientes no hospitalizados con claudicación intermitente. Estudio aleatorio controlado / A study of the clinical and analytical repercussions of a nutritional intervention in non-hospitalised patients with intermittent claudication. A controlled randomised study

Introducción. La dieta es un pilar fundamental, a veces olvidado, en el control y tratamiento de la enfermedad vascular periférica (EVP). Objetivo. Estudiar los efectos de la ingesta de ciertos nutrientes con probado efecto beneficioso en la prevención de la enfermedad coronaria en la clínica y el perfil bioquímico de enfermos claudicantes. Pacientes y métodos. Estudio longitudinal, descriptivo, aleatorio y doble ciego, con 60 varones claudicantes (grado IIB de Fontaine), distribuidos en dos grupos. Grupo I (n = 30): además de su dieta habitual consumieron 500 mL/día de leche semidesnatada adicionada de ácidos eicosapentanoico, docoxahexanoico, oleico y fólico y vitaminas A, D, E y B6. Grupo C (n = 26): además de su dieta habitual consumieron 500 mL/día de leche semidesnatada. Ambos grupos obtuvieron los mismos consejos higienicodietéticos, un antiagregante plaquetario (triflusal) y un hemorreológico (pentoxifilina). Con control trimestral, la intervención duró 12 meses. En cada control se realizó una exploración clínica vascular, claudicometría, índice de Yao, placetismografía y analítica. Resultados. La concentración plasmática de los nutrientes suministrados aumentó en el grupo I (p < 0,05), seguido de un descenso en colesterol total y la concentración de apolipoproteína B. La homocisteína total disminuyó en aquellos pacientes con hiperhomocisteinemia (p < 0,01). Paralelamente, la distancia de claudicación triplicó su valor (p < 0,001) y el índice de Yao aumentó de manera gradual (p < 0,05). Conclusiones. La inclusión diaria en la dieta de ciertos nutrientes cardiosaludables produjo, junto con otras recomendaciones dietéticas y hábitos de vida, una mejora significativa en los parámetros clínicos y analíticos de este grupo de claudicantes. La nutrición puede desempeñar un papel importante en el tratamiento y control de la EVP

INTRODUCTION. Diet is a sometimes neglected cornerstone in the control and treatment of peripheral vascular disease (PVD). AIMS. To study how the intake of certain nutrients with a proven beneficial effect in the prevention of heart disease affects the clinical symptoms and biochemical profile of patients with claudication. PATIENTS AND METHODS. A longitudinal, descriptive, randomised, double-blind study was conducted with 60 males with claudication (Fontaine grade IIB), distributed in two groups. Group I (n = 30): in addition to their usual diet, subjects consumed 500 ml/day of semi-skimmed milk with added eicosapentaenoic, docosahexaenoic, oleic and folic acids, as well as vitamins A, D, E and B6. Group C (n = 26): in addition to their usual diet, subjects consumed 500 mL/day of semi-skimmed milk. Both groups received the same hygienic-dietary guidelines, an antiplatelet drug (triflusal) and a haemorrheologic agent (pentoxifylline). Including a three-monthly control, the intervention lasted 12 months. At each control the following tests were carried out: vascular clinical examination, treadmill exercise testing, Yao index, plethysmography and analyses. RESULTS. The plasma concentration of the nutrients given to patients increased in group I (p < 0.05), followed by a decrease in total cholesterol and apolipoprotein B concentration. The total homocysteine level dropped in patients with hyperhomocysteinemia (p < 0.01). In a parallel fashion, the claudication distance become three times longer (p < 0.001) and the Yao index gradually increased (p < 0.05). CONCLUSIONS. Including certain nutrients that are good for the heart in the daily diet, along with other guidelines concerning nutrition and lifestyle, led to a significant improvement in the clinical and analytical parameters of this group of patients with claudication. Nutrition can play an important role in the treatment and control of PVD

Optimization of daily folate, vitamin B12 and vitamin B6 supplements in paediatric patients with sickle cell disease

We determined optimal folate, vitamin B12 and vitamin B6 dosages in 21 sickle cell disease (SCD) patients (11 HbSS, 10 HbSC; mean 7 years, range 7-16), using plasma homocysteine (Hcy) as functional marker. They received daily 400 g (0-3 weeks), 700 g (3-6) and 1000 g (6-70) folate; 1 (0-21), 3 (21-45 and 5 RDA (45-70) vitamin B12; and 1 RDA vitamin B6 (0-70). Blood was taken at baseline (P0) and after 3 (PI), 6 (P2), 9 (P3), 21 (P4), 33 (P5), 45 (P6), 57 (P7) and 70 (P8) weeks for measurement of erythrocyte (RBC), serum folate, plasma vitamin B12, whole blood vitamin B6 and plasma Hcy. Vitamin B6 increased from P0 to P1 and P1 to P2; vitamin B12 from P4 to P8; serum folate from P0 to P1 and P1 to P2; RBC folate from P0 to P1, P1 to P2 and P2 to P3. Hcy decreased from P1 to P2 and P4 to P6. Most pronounced Hcy decreases occurred from P0 to P1 (43 percent of patients), P1 to P2 (14 percent) and P4 to P5 (24 percent). Haematological indices did not change. Patients with HbSS had higher RBC folate at P1, P2 and P8. The entire group exhibited inverse relations between RBC folate and haemoglobin on P1, P2, P3, P6, P7 and P8. We conclude that RBC folate is less valuable for folate status assessment in SCD patients. The optimal daily supplement is 700 g folate (3.5-7 RDA vitamin B12 (4.2-6.0 g) and 1 RDA vitamin B6 (1.4-2.0 mg). This combination causes Hcy levels that do not decrease further upon higher dosages and may reduce by simple and relatively inexpensive means their inherently high risk of endothelial damage.(Au)

Mice lacking tissue non-specific alkaline phosphatase die from seizures due to defective metabolism of vitamin B-6.

In humans, deficiency of the tissue non-specific alkaline phosphatase (TNAP) gene is associated with defective skeletal mineralization. In contrast, mice lacking TNAP generated by homologous recombination using embryonic stem (ES) cells have normal skeletal development. However, at approximately two weeks after birth, homozygous mutant mice develop seizures which are subsequently fatal. Defective metabolism of pyridoxal 5'-phosphate (PLP), characterized by elevated serum PLP levels, results in reduced levels of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the brain. The mutant seizure phenotype can be rescued by the administration of pyridoxal and a semi-solid diet. Rescued animals subsequently develop defective dentition. This study reveals essential physiological functions of TNAP in the mouse.

[The vitamin B6 allowance of hypertension patients and the effect of dietotherapy]. / Obespechennost' vitaminom B6 bol'nykh gipertonicheskoi bolezn'iu i vliianie dietoterapii.

A total of 111 patients with essential hypertension (the II stage) and obesity (the II degree) were investigated for providing with vitamin B6. The functional methods used for the vitamin assay (ACT activity of red blood cells and pyrodoxale-5-phosphate effect) have revealed significant vitamin B6 deficiency in 81.1% of the patients. Vitamin B6 deficiency was intensified in the course of the dietotherapy. Correction of vitamin B6 deficiency with a therapeutic dose of pyridoxine (20 mg/day) during 20-22 days, in the presence of the diet, has promoted optimization of providing with vitamin B6: normalization of pyrodoxale-5-phosphate effect. The hypotensive effect and decrease of excessive body mass in patients who received dietotherapy and pyridoxine (20 mg/day) were more pronounced than in those who received the same diet and the multivitamin "Undevitum".