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.

中文翻译：

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母体维生素 B12 从妊娠末期到断奶期间缺乏对母鼠和后代生长、血液学和免疫学参数的影响

维生素 B12 缺乏可能会引起特定症状，如神经系统改变和非特异性症状，如贫血和生长迟缓。在这项研究中，评估了母鼠从妊娠末期到断奶期间维生素 B12 缺乏的情况，这是由喂养缺乏维生素 B12 的饮食引起的。将动物分成两组（对照组和缺陷组）。对照组接受补充有商业维生素 B12 的缺乏维生素 B12 的饮食。与对照组相比，缺乏维生素 B12 的母鼠及其后代的体重（分别下降 20% 和 39%）、血清维生素 B12 浓度（分别下降 61% 和 67%）、血液学值作为血细胞比容均显着下降（ 25% 和 26%）和 IgA 生产细胞（分别为 36% 和 54%）。同时，在缺乏维生素 B12 的小鼠水坝及其后代中，观察到小肠的组织学改变，而仅在后代中发生生长迟缓。这种实验性小鼠模型可以评估后代中母体钴胺素缺乏症的发生率，并可用于评估新的辅助食品，如功能性食品，以防止维生素 B12 缺乏症。