Anzano M A, Lamb A J, Olson J A
J Nutr. 1979 Aug;109(8):1419-31. doi: 10.1093/jn/109.8.1419.
Experiments were conducted to determine the sequence and reliability of appearance of key signs of vitamin A deficiency. Rapid and essentially synchronous vitamin A deficiency was induced by the withdrawal of retinoic acid from mature (190--210 g) stringently vitamin A-deficient male rats reared by feeding early growth plateau (60--70 g) vitamin A-deprived rats diets first supplemented with and then lacking in 2 micrograms retinoic acid per gram diet in repeating 18 day:10 day supplementation:deprivation cycles. Growth was depressed within 1 to 2 days of the withdrawal of retinoic aicid whether animals were force-fed or were fed ad libitum. Similar patterns were obtained when animals were fed 5 or 10 micrograms retinoic acid per gram diet. Appetite was depressed (1--2 days) whether animals were fed 18% casein diets, or were given 10% dextrose drinking solutions only. Decreased food intake was not due to impaired taste function or to poor palatability of the deficient diet. Bilateral electrolytic lesions in the ventromedial nucleus of the hypothalamus or anterior prepyriform cortex failed to prevent or to delay loss of appetite. Supplementation with antibiotics decreased body weight losses in the late stages of deficiency and increased survival time. Other signs of deficiency (days until onset following retinoate withdrawal; percent incidence) were: decreased intestinal goblet cell numbers (2--3; 80), decreased pilocarpine induced salivation (6--8; 80), tracheal metaplasia (6--8; 80), transient periocular porphyria (6--8; 60), altered salivary gland morphology (9--10; 80), decreased stomach emptying in force-fed animals (12; 70), twisting (12; 5) and leg crippling (12; 5). We conclude that the sequence of appearance of individual signs of deficiency following the induction of synchronous vitamin A deficiency is highly reproducible, and that the more general use of synchronously deficient animals would materially assist studies of cause-effect relationships in vitamin A deficiency.
开展了实验以确定维生素A缺乏关键体征出现的顺序和可靠性。通过从成熟（190 - 210克）严格维生素A缺乏的雄性大鼠中撤去视黄酸来诱导快速且基本同步的维生素A缺乏，这些大鼠是由早期生长稳定期（60 - 70克）的维生素A缺乏大鼠饲养而来，其饮食先补充每克含2微克视黄酸，然后缺乏视黄酸，重复18天补充：10天缺乏的周期。无论动物是强制喂食还是自由采食，在撤去视黄酸后的1至2天内生长都会受到抑制。当动物喂食每克含5或10微克视黄酸的饮食时，也会得到类似的模式。无论动物喂食18%酪蛋白饮食，还是仅给予10%葡萄糖饮用溶液，食欲都会受到抑制（1 - 2天）。食物摄入量减少并非由于味觉功能受损或缺乏饮食的适口性差。下丘脑腹内侧核或前梨状皮质的双侧电解损伤未能预防或延迟食欲丧失。补充抗生素可减少缺乏后期的体重减轻并延长存活时间。其他缺乏体征（撤去视黄酸酯后直至出现的天数；发生率百分比）如下：肠杯状细胞数量减少（2 - 3天；80%）、毛果芸香碱诱导的唾液分泌减少（6 - 8天；80%）、气管化生（6 - 8天；80%）、短暂性眼周卟啉症（6 - 8天；60%）、唾液腺形态改变（9 - 10天；80%）、强制喂食动物胃排空减少（12天；70%）、扭体（12天；5%）和腿部跛行（12天；5%）。我们得出结论，在诱导同步维生素A缺乏后，个体缺乏体征出现的顺序具有高度可重复性，并且更广泛地使用同步缺乏动物将极大地有助于维生素A缺乏因果关系的研究。
