Dileepan K N, Singh V N, Ramachandran C K
J Nutr. 1977 Oct;107(10):1809-15. doi: 10.1093/jn/107.10.1809.
In an earlier report from this laboratory, one of the early manifestations of hypervitaminosis A was shown to be a marked stimulation of hepatic gluconeogenesis. In the present study, effects of feeding 30,000 IU of retinyl palmitate to young rats (80-100 g), once daily, for 2 days on the incorporation of 14C-labeled precursors into glucose and glycogen by liver slices, levels of amino acids in blood and tissues, and activities of some important amino acid catabolizing enzymes in the liver were investigated. A stimulation of hepatic gluconeogenesis in hypervitaminosis A was indicated by the increased incorporation of 14C-labeled alanine and bicarbonate into glucose and glycogen by liver slices. Excessive intake of retinol caused a marked increase in the activities of hepatic alanine aminotransferase and ornithine aminotransferase and a decrease in that of tryptophan pyrrolase, without affecting those of tyrosine aminotransferase and serine dehydratase. The ratio of NADH:NAD in the livers of rats fed excess retinol was significantly increased. It is suggested that enhancement of glucoeogenesis in hypervitaminosis A is caused by a stimulation of gluconeogenic activity of the liver.
在本实验室早期的一份报告中,维生素A过多症的早期表现之一被证明是肝脏糖异生显著增强。在本研究中,对80 - 100克的幼鼠每天喂一次30,000国际单位的棕榈酸视黄酯,持续2天,研究其对肝切片将14C标记的前体掺入葡萄糖和糖原、血液和组织中氨基酸水平以及肝脏中一些重要氨基酸分解代谢酶活性的影响。肝脏切片将14C标记的丙氨酸和碳酸氢盐掺入葡萄糖和糖原增加,表明维生素A过多症时肝脏糖异生增强。过量摄入视黄醇导致肝脏丙氨酸转氨酶和鸟氨酸转氨酶活性显著增加,色氨酸吡咯酶活性降低,而对酪氨酸转氨酶和丝氨酸脱水酶活性无影响。喂食过量视黄醇的大鼠肝脏中NADH:NAD的比值显著增加。提示维生素A过多症时糖异生增强是由肝脏糖异生活性增强引起的。