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维生素 A 缺乏症会增加蛋白质的分解代谢,并诱导大鼠的尿素循环酶。

Vitamin A deficiency increases protein catabolism and induces urea cycle enzymes in rats.

机构信息

Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Valencia, Valencia, Spain.

出版信息

J Nutr. 2010 Apr;140(4):792-8. doi: 10.3945/jn.109.119388. Epub 2010 Feb 24.

DOI:10.3945/jn.109.119388
PMID:20181784
Abstract

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.

摘要

慢性维生素 A 缺乏症会导致人类和实验动物的体重和身高增长速度明显减慢。这种影响与营养物质代谢受损和身体蛋白质流失有关。因此,我们分析了维生素 A 缺乏症对内源性蛋白水解和氮代谢的影响,以及全反式视黄酸(RA)对其的逆转作用。雄性断奶大鼠成对饲养,接受维生素 A 缺乏(VAD)或对照饮食喂养,直到 60 日龄。一组缺乏症大鼠进一步接受每日腹腔注射全反式 RA 治疗 10 天。VAD 大鼠的最终体重和组织(即肝脏和心脏)重量显著降低,组织与体重的比值与对照组相似。相反,VAD 大鼠的附睾白色脂肪与体重的比值以及丙氨酸氨基转移酶和脂联素的血浆浓度显著升高,且肝脏存在大泡性脂肪堆积。VAD 组的血浆和比目鱼肌 3-甲基组氨酸、尿氮以及血浆和尿中尿素浓度均显著升高。VAD 肝脏中编码尿素循环酶的基因表达及其活性增加。全反式 RA 部分逆转了这些变化。我们提出,在维生素 A 缺乏症中,燃料分配可能从脂肪酸转移到蛋白质分解代谢作为能量来源。我们的结果强调了维生素 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。

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