Molina Verónica, Medici Marta, Taranto María Pía, Font de Valdez Graciela
Centro de Referencia para Lactobacilos (CERELA-CONICET), San Miguel de Tucumán, Argentina.
Arch Anim Nutr. 2008 Apr;62(2):162-8. doi: 10.1080/17450390801892567.
Vitamin B12-deficiency may induce specific symptoms as neurological alterations and unspecific symptoms such as anaemia and growth retardation. In this study, maternal vitamin B12 deficiency from end of gestation to weaning was evaluated in mouse dams, which was provoked by feeding a vitamin B12-deficient diet. The animals were divided into two groups (control and deficient). The control group received the vitamin B12-deficient diet supplemented with commercial vitamin B12. Compared to the control, the vitamin B12-deficient dams and their offspring showed a significant decrease of body weight (by 20 and 39%, respectively), serum vitamin B12 concentration (by 61 and 67%, respectively), haematological values as haematocrit (25 and 26%, respectively), and IgA producer cells (by 36 and 54%, respectively). In both, vitamin B12-deficient mouse dams and their offspring, histological alterations of small intestine were observed, whereas growth retardation occurred in the offspring only. This experimental murine model allows assessing the incidence of maternal cobalamin deficiency in offspring and would be useful for evaluating novel adjuncts such as functional foods to prevent vitamin B12 deficiency.
维生素B12缺乏可能引发特定症状,如神经功能改变,以及非特异性症状,如贫血和生长发育迟缓。在本研究中,通过给母鼠喂食缺乏维生素B12的饮食,诱发其从妊娠末期到断奶期间维生素B12缺乏,对母鼠进行了评估。将动物分为两组(对照组和缺乏组)。对照组接受补充了商业维生素B12的缺乏维生素B12的饮食。与对照组相比,缺乏维生素B12的母鼠及其后代体重显著下降(分别下降20%和39%),血清维生素B12浓度显著降低(分别降低61%和67%),血液学指标如血细胞比容(分别降低25%和26%)以及IgA产生细胞(分别降低36%和54%)。在缺乏维生素B12的母鼠及其后代中,均观察到小肠的组织学改变,而生长发育迟缓仅发生在后代中。这种实验性小鼠模型有助于评估后代中母体钴胺素缺乏的发生率,并且对于评估新型辅助手段,如功能性食品以预防维生素B12缺乏将是有用的。