Search

We investigated the efficacy of supplementing the diet with choline or betaine in ameliorating lipid accumulation induced by vitamin B6(B6) deficiency in rat liver. Male Wistar rats were fed a control, B6-deficient, choline-supplemented (2, 4, or 6 g choline bitartrate/kg diet) B6-deficient diet or betaine-supplemented (1, 2, or 4 g betaine anhydrous/kg diet) B6-deficient diet for 35 d; all diets contained 9 gL-methionine (Met)/kg diet. Choline or betaine supplementation attenuated liver lipid deposition and restored plasma lipid profiles to control levels. These treatments restored the disruptions in Met metabolism and the phosphatidylcholine (PC)/phosphatidylethanolamine (PE) ratio induced by B6deficiency in liver microsomes. These results suggest that choline and betaine ameliorated liver lipid accumulation induced by B6deficiency via recovery of Met metabolism and very low-density lipoprotein secretion by restoring the supply of PC derived from PE. Choline and betaine ameliorate liver lipid accumulation induced by vitamin B6deficiency through normalization of disturbed methionine metabolism. [ABSTRACT FROM AUTHOR]

The article presents the findings of a research conducted on evaluating the effects of Vitamin B6 deficiency, levels of dietary methionine and fortified folate on the homocysteine metabolism. It discusses the methodology used in conducting the research including statistical analysis, high performance liquid chromatography and ultraviolet detection. The research reveals that folate fortification ameliorates the hyperhomocysteinemia.

Abstract: The incidence of type I diabetes is rising worldwide, particularly in young children. Type I diabetes is considered a multifactorial disease with genetic predisposition and environmental factors participating. Currently, despite years of research, there is no consensus regarding the factors that initiate the autoimmune response. Type I diabetes is preceded by autoimmunity to islet antigens, among them the protein glutamic acid decarboxylase, GAD-65. Pyridoxal 5’-phosphate (PLP) is formed from vitamin B6 by the action of pyridoxal kinase. Interaction of GAD65 with PLP is necessary for GAD65-mediated synthesis of the neurotransmitter γ-aminobutyric acid (GABA). PLP is also a required cofactor for dopamine synthesis by L-aromatic decarboxylase (L-AADC). Both GAD65 and L-AADC are expressed in pancreatic islets. Here it is proposed that lack of the vitamin B6 derivative pyridoxal 5’-phosphate might contribute to the appearance of pancreatic islet autoimmunity and type I diabetes onset. [Copyright &y& Elsevier]

Abstract: Purpose: Pyridoxine-Dependent Epilepsy (PDE) is a rare autosomal recessive disease with neonatal seizures resistant to conventional anti-epileptic drugs. This metabolic disease has to be diagnosed early and treated to improve outcome. We report on two new mutations that open new prenatal prospects and suggest a new diagnostic procedure. Case report: We describe PDE in a neonate carrying two novel mutations in the ALDH7A1 gene: c.[852_856delCTTAG] + [1230C > A]; p.[(Phe410Leu)] + p.[(Leu285CysfsX26)]. This case also illustrates that diagnosis could have been made without any pyridoxine withdrawal, thanks to the measurement of biomarkers. The patient was successfully treated with pyridoxine supplementation and currently shows normal neurological development. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: We investigated the effect of a vitamin B6 deficiency and pair-feeding on tissue trace element status. Method: Tissue zinc, copper and iron concentrations were measured in 3 groups of young, male Wistar rats receiving a diet of 3.5mg/kg (control group), 0mg/kg (deficient group) and a pair-fed group over 8 weeks. The pair-fed group received the same diet consumed by the control. Tissue trace element analysis was performed using atomic absorption spectrophotometry and plasma vitamin B6 status was determined using HPLC. Results: Deficiency resulted in elevation in liver iron concentration and reduction in muscle iron concentration. Muscle copper concentrations were reduced in the pair-fed and deficient groups vs. the control group. Tissue zinc concentrations remained unaffected by the deficiency. Kidney iron and heart copper levels were elevated in the pair-fed group. Conclusions: The liver and muscle iron changes were due to the deficiency and not to reduced calorie intake and the latter may be due to impaired heme synthesis. The differences in copper between the groups were due to reduced food intake. Zinc seems to form a fixed pool in these animals. A dietary deficiency of vitamin B6 impacts on the trace element status of certain tissues in key metabolic tissues and hence needs to be factored into the amelioration of the condition. [Copyright &y& Elsevier]

Summary: Background and aims: The aim of this study was to evaluate the lipid peroxidation and antioxidant function in liver tissue of vitamin B6 deficient rats and investigate relationship among these parameters in either group. Methods: Twenty-four male rats with a weight of 48–59g were used for the experiment. The rats were divided into control () and vitamin B6 deficient groups. After 4 weeks of feeding, the rats were killed by cervical dislocation and liver tissues were removed. Biochemical measurements in liver tissue were carried out using a spectrophotometer. Results: Liver tissue antioxidant potential, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, total (enzymatic plus non-enzymatic) superoxide scavenger activity, non-enzymatic superoxide scavenger activity, glutathione levels were significantly lower in vitamin B6 deficient rats than in control group. However, liver tissue glutathione reductase activity, and MDA values were significantly higher in vitamin B6 deficient rats than in control group. Conclusions: These results explicitly indicate that vitamin B6 deficiency causes a decrease in antioxidant defense system and an increase in oxidant stress in liver tissue in rats. [Copyright &y& Elsevier]

The article informs that a variety of evidence suggests altered vitamin B[sub6] metabolism in Down's syndrome. Studies using deoxypyridoxine suggested that the vitamin B[sub6] pool was either reduced or turned over more rapidly in Down's syndrome than in controls. When individuals with Down's syndrome were given 350 mg pyridoxine hydrochloride per day, the concentration of pyridoxal phosphate in plasma was significantly higher than in controls receiving the same intake. Therefore, the regulation of pyridoxal phosphate concenrations in plasma appears to be altered in Down's syndrome.

The article investigates the nutritional needs of mentally retarded individuals in the U.S. Nervous system illnesses often involve some aspect of vitamin B6 function. Patients with Down syndrome were found to have a decrease serotonin levels which could be a manifestation of the decrease in vitamin B6 function. The investigators advised adult males to take vitamin B6 at 2.2 milligrams and 2.0 milligrams for adult females. However, vitamin B6 deficiency due to dietary deficit is considered rare.