Kennedy D G, Young P B, McCaughey W J, Kennedy S, Blanchflower W J
Department of Biochemistry, Veterinary Research Laboratories, Belfast, Northern Ireland, United Kingdom.
J Nutr. 1991 Aug;121(8):1236-42. doi: 10.1093/jn/121.8.1236.
When lambs were fed a cobalt-deficient whole barley diet there was a rapid and massive increase in rumen succinate concentrations. Within 2 d of feeding the Co-deficient diet, the rumen succinate concentrations rose 200-fold and peaked at a level 1000-fold higher than that in Co-sufficient controls. Rumen propionate concentrations decreased, suggesting that an alteration in the balance between succinate- and propionate-producing microorganisms had occurred. The rumen succinate can be absorbed and thus may lead to elevated plasma succinate concentrations in Co-deficient animals, whether fed barley or grass. Thus, the absorbed succinate can at least partially overcome the effect on gluconeogenesis of a decreased activity of methylmalonyl CoA mutase induced by Co-deficiency. These findings suggest that impaired propionate metabolism may not be the primary metabolic defect in ovine Co-deficiency.
当给羔羊饲喂缺钴的整粒大麦日粮时，瘤胃琥珀酸浓度迅速大幅增加。在饲喂缺钴日粮的2天内，瘤胃琥珀酸浓度升高了200倍，达到比钴充足对照组高1000倍的峰值。瘤胃丙酸浓度降低，表明琥珀酸产生菌和丙酸产生菌之间的平衡发生了改变。瘤胃琥珀酸可以被吸收，因此可能导致缺钴动物（无论饲喂大麦还是青草）血浆琥珀酸浓度升高。因此，吸收的琥珀酸至少可以部分克服钴缺乏诱导的甲基丙二酰辅酶A变位酶活性降低对糖异生的影响。这些发现表明，丙酸代谢受损可能不是绵羊钴缺乏的主要代谢缺陷。
