Vitamin A Deficiency Increases Protein Catabolism and Induces Urea Cycle Enzymes in Rats
Vitamin A Deficiency Increases Protein Catabolism and Induces Urea Cycle Enzymes in Rats
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DOI：
10.3945/jn.109.119388
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发表时间：
2010-04-01
影响因子：
4.2
通讯作者：
Barber, Teresa
中科院分区：
文献类型：
--
作者：
Esteban-Pretel, Guillermo;Pilar Marin, M.;Barber, Teresa
慢性维生素A缺乏会导致人类和实验动物体重和身高增加率的显著延迟。这种影响与营养代谢受损和身体蛋白质损失有关。因此，我们分析了维生素A缺乏对内源性蛋白水解和氮代谢的影响及其与全反式维甲酸（RA）的可逆性。雄性断乳大鼠，成对饲养，成对喂养维生素A缺乏（VAD）或对照饮食，直到他们60日龄。另一组大鼠继续腹腔注射全反式维甲酸10 d。VAD大鼠和对照组的最终体重和组织（即肝脏和心脏）重量显著降低，组织：体重比相似。相反，VAD大鼠的附睾白色脂肪：体重比以及丙氨酸氨基转移酶和脂联素的血浆浓度显著较高，也有肝大泡脂质蓄积。血浆和腓肠肌3-甲基组氨酸，尿氮，血浆和尿尿素浓度都显着较高的VAD组。在VAD肝脏中，尿素循环酶编码基因的表达及其活性增加。这些变化被全反式RA部分逆转。我们建议，维生素A缺乏症的燃料分配可能会从脂肪酸转移到蛋白质催化剂作为能源。我们的研究结果强调了维生素A对能量平衡控制系统的重要性，并为维生素A在蛋白质周转、发育和生长中的作用提供了解释。J.营养140：792-798，2010.
Chronic vitamin A deficiency induces a substantial delay in the rates of weight and height gain in both humans and experimental animals. This effect has been associated with an impaired nutrient metabolism and loss of body protein. Therefore, we analyzed the effect of vitamin A deficiency on endogenous proteolysis and nitrogen metabolism and its reversibility with all-trans retinoic acid (RA). Male weanling rats, housed in pairs, were pair-fed a vitamin A-deficient (VAD) or control diet until they were 60 d old. A group of deficient rats were further treated with daily intraperitoneal injections of all-trans RA for 10 d. Final body and tissue (i.e. liver and heart) weights were significantly lower and tissue:body weight ratios were similar in VAD rats and in controls. Conversely, the epididymal white fat:body weight ratio and the plasma concentrations of alanine aminotransferase and adiponectin were significantly higher in VAD rats, which also had hepatic macrovesicular lipid accumulations. Plasma and gastrocnemius muscle 3-methylhistidine, urine nitrogen, and plasma and urine urea concentrations were all significantly higher in the VAD group. The expression of the genes encoding urea cycle enzymes and their activities increased in VAD livers. These changes were partially reverted by all-trans RA. We propose that fuel partitioning in vitamin A deficiency may shift from fatty acids to protein catabolism as an energy source. Our results emphasize the importance of vitamin A on the energy balance control system and they provide an explanation for the role of vitamin A in protein turnover, development, and growth. J. Nutr. 140: 792-798, 2010.