Stangl G I, Schwarz F J, Kirchgessner M
Institut für Ernährungsphysiologie, Technische Universität München, Freising-Weihenstephan, Germany.
Int J Vitam Nutr Res. 1999 Mar;69(2):120-6. doi: 10.1024/0300-9831.69.2.120.
This study was conducted to investigate the physiological consequences of long-term moderate cobalt deficiency in beef cattle, which have not hitherto been studied in detail. Cobalt deficiency was induced in cattle by feeding two groups of animals either a basal corn silage-based diet that was moderately low in cobalt (83 micrograms Co/kg), or the same diet supplemented with cobalt to a total of 200 micrograms per kg, for 43 weeks. Cobalt deficiency was induced, as judged by inappetance, diminished growth gain and a markedly reduced vitamin B12 status in serum and liver. The long-term cobalt deprivation which was primarily a combination of reduced feed intake and a tissue vitamin B12 deficiency did not show evidence of a significant dysfunction of energy metabolism. The activities of glucose-6-phosphate dehydrogenase and cytochrome oxidase in liver remained unaffected by cobalt deficiency, nor was there a significant change in serum glucose level of cattle on the cobalt-deprived diet. However, analysis of thyroid hormone status indicated a slight reduction of type I thyroxine monodeiodinase activity in liver accompanied by a significant reduction of the triiodothyronine level in serum. The diminished liver vitamin B12 level resulted in significantly reduced folate level in this tissue, reduced concentrations of heme-depending blood parameters. Moreover cobalt deficiency or rather vitamin B12 deficiency was accompanied by a dramatic accumulation of the trace elements iron and nickel in liver. These results indicate that long-term moderate cobalt deficiency may induce a number of physiological changes in cattle, but a follow-up study, which excluded different feed levels by including a pair-fed control group, will be necessary to actually obtain the single effect of cobalt deficiency in cattle.
本研究旨在调查肉牛长期中度钴缺乏的生理后果，此前尚未对此进行过详细研究。通过给两组动物喂食两种日粮来诱导钴缺乏，一组喂食以玉米青贮为基础的日粮，钴含量适度较低（83微克钴/千克），另一组喂食相同日粮但添加钴使总量达到每千克200微克，持续43周。根据食欲不振、生长增重减少以及血清和肝脏中维生素B12水平显著降低来判断钴缺乏已被诱导。长期的钴缺乏主要是饲料摄入量减少和组织维生素B12缺乏的综合结果，未显示出能量代谢明显功能障碍的证据。肝脏中葡萄糖-6-磷酸脱氢酶和细胞色素氧化酶的活性不受钴缺乏的影响，钴缺乏日粮组牛的血清葡萄糖水平也没有显著变化。然而，甲状腺激素状态分析表明，肝脏中I型甲状腺素单脱碘酶活性略有降低，同时血清中三碘甲状腺原氨酸水平显著降低。肝脏维生素B12水平降低导致该组织中叶酸水平显著降低，血红素相关血液参数浓度降低。此外，钴缺乏或更确切地说是维生素B12缺乏伴随着肝脏中铁和镍等微量元素的大量积累。这些结果表明，长期中度钴缺乏可能会在牛身上引发一些生理变化，但有必要进行一项后续研究，通过纳入配对饲喂对照组来排除不同饲料水平的影响，以实际获得钴缺乏对牛的单一影响。
