These data might indicate that diabetic animals should have a higher intake of vitamin B6 because a diabetic state can lead to a vitamin B6-deficiency.

SummaryRats were fed 20 or 70% casein diets with varying amounts of vitamin B6 (B6), and the B6 content and B6-dependent enzymatic activity in their tissues were examined to determine the minimum re quirement of B6 for animals subjected to different levels of dietary protein (i.e., 20%: 0, 1.45, 2.90, 5.80mg pyridoxine (PN)/kg diet; 70%: 0, 2.90, 5.80, 8.70mg PN/kg diet). B6 requirements for the rats were almost met in the 1.45mg PN/kg 20% casein diet and the 2.90mg PN/kg 70% casein diet when judged from the hepatic B6 content. However, almost twice the PN was required in both 20 and 70% casein diets when judged from PLP-enzymatic activity. The content of B6 vitamers in plasma appeared to be most sensitive to B6 status, though the satisfactory level is not known. It was confirmed that, in any case tested, a high-protein diet increased the requirement of B6. Key Words vitamin B6 requirement, vitamin B6 content, aspartate aminotransferase, glycogen phosphorylase Vitamin B6 (B6) is found in biological tissues and fluids as pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM) and their phosphorylated derivatives. The vitamers function as coenzymes of glycogen phosphorylase and many amino acid metabolic enzymes. A high-protein diet increases the requirement for B6 as follows: First, a high-protein diet containing a low B6 content increases the urinary excre tion of xanthrenic acid (an abnormal metabolite of tryptophan) and some other tryptophan metabolites such as kynurenine and hydroxykynurenine (1); second, in animals fed a B6-free, high-protein diet, growth is retarded and is accompanied by a severe decrease in the activity of pyridoxal enzymes compared to animals fed a B6-free, low-protein diet (2, 3); and third, an increase in B6 intake increases phosphorylated pyridoxal (PLP) concentration, whereas increased protein intake decreases plasma PLP concentration (4).The accurate determination of B6 in biological samples is essential for assessing nutritional and metabolic requirements. There have been many attempts to analyze

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73Branched-chain amino acids (BCAAs) composed of valine, leucine, and isoleucine are essential amino acids and account for about 40% of dietary essential amino acids in body protein and about 15% of total amino acids in muscle proteins (1). BCAAs play a role in delayed onset of muscle soreness and fatigue, and suppression of fatigue in the central nervous system (2, 3). BCAAs have been also used for the prevention of hepatic encephalopathy in patients with liver cirrhosis (4, 5). Recently, sport enthusiasts have created an increased demand for dietary supplements with BCAAs and have increased their consumption of BCAAs-enriched soft drinks.The first step in the catabolism of BCAAs involves branched-chain aminotransferase (BCAT; EC 2.6.1.42), a common enzyme. This enzyme requires vitamin B 6, which functions as a cofactor in many enzyme reactions of amino acid metabolism (6, 7). However, little information is available on the relationship between supplementation with BCAAs and the recommended daily allowance of vitamin B6. In addition, it is known that a high-protein diet (e.g., 70% casein diet) under vitamin B6 deficiency has a negative impact on several biochemical parameters and leads to fatty liver in rats (8-10).Our previous study showed that providing supplemented BCAAs under vitamin B6 deficiency and a 20% casein diet caused an accumulation of triacylglycerol in the liver, and individual differences in biological responses were observed (11). It is possible that a disorder of amino acid metabolism in the presence of vitamin B6 deficiency might influence the assembly of lipids and apolipoproteins and/or the secretion of lipoproteins. Among the serum lipoproteins, very low-density lipoprotein (VLDL) is present during endogenous lipogenesis in the liver and its major apolipoproteins are apolipoprotein (apo) B, apo C, and apo E (12). It is interesting to compare serum apo B and apo E levels, and hepatic apoE levels to evaluate lipid deposition, because apo B and apo E are key determinants responsible for cellular recognition and internalization of chylomicron remnants, VLDL, and high-density lipoprotein (HDL) (13,14). In this study, we investigated the possible mechanism of lipid deposition in the liver of rats fed with the supplementation of BCAA under vitamin B 6 deficiency and suggested the presence of impaired secretion of VLDL into the bloodstream from the liver. Materials and MethodsDiets and animals. Four diets composed of purified 20% vitamin-free casein diet with (1) or without (2) vitamin B6 (7.0 mg of pyridoxine HCl/kg of diet) and with (1) or without (2) Summary Male Wistar rats were fed four diets composed of purified 20% vitamin-free casein diet with (1) or without (2) vitamin B6 (7.0 mg of pyridoxine HCl/kg of diet) and with (1) or without (2) branched-chain amino acids (BCAAs) of valine, leucine, and isoleucine (4.75%): B6 (1)BCAA (2); B6(1)BCAA(1); B6 (2)BCAA (2); and B6 (2)BCAA (1) for 21 d. Among rats fed the B6(2)BCAA(1) diet, about a half showed lipid deposition in the liver. On the other...