High Incidence of Lipid Deposition in the Liver of Rats Fed a Diet Supplemented with Branched-Chain Amino Acids under Vitamin B6 Deficiency

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Male Wistar rats were fed four diets composed of purified 20% vitamin-free casein diet with (+) or without (−) vitamin B6 (7.0 mg of pyridoxine HCl/kg of diet) and with (+) or without (−) branched-chain amino acids (BCAAs) of valine, leucine, and isoleucine (4.75%): B6(+)BCAA(−); B6(+)BCAA(+); B6(−)BCAA(−); and B6(−)BCAA(+) for 21 d. Among rats fed the B6(−)BCAA(+) diet, about a half showed lipid deposition in the liver. On the other hand, serum triacylglycerol levels in the B6(−)BCAA(+) group tended to be decreased. Hepatic triacylglycerol and cholesterol levels tended to increase in the B6(−)BCAA(+) group compared with the other three groups. Serum apolipoprotein B and apolipoprotein E (apo E) levels in the B6(−)BCAA(+) group were the lowest among the three groups. In contrast, hepatic apo E levels in the B6(−)BCAA(+) group were the highest among the three groups. High-performance liquid chromatography of pooled serum of rats with lipid deposits revealed that triacylglycerol and cholesterol levels in very low-density lipoprotein (VLDL) were decreased compared with other diet groups. These results strongly suggest that one of the mechanisms of lipid deposition in rats fed a B6(−)BCAA(+) diet is due to impaired secretion of VLDL.