基于代谢组学探讨犊牛失明原因.

[Objective] The present paper aimed to further study the causes of calf blindness aud provide theoretical support for reducing the incidence of congenital blindness of calves aud reducing the economic losses of the breeding industry. [ Method] A cattle farm was selected in Ningxia, whose birth date was close to that of blind calves aud their mothers, aud normal calves. Blood and plasma samples were collected. Through metabonomic aualysis, the differential metabolites and pathway changes between blind calves and their mothers, aud normal calves were studied. [Result] The VIP value of OPLS-DA > 1 and the univariate statistical aualysis P < 0. 05 were used as the criteria for significautly different metabolites. A total of 256 different metabolites were screened from the comparison group of blind calves and normal calves ( V aS. vs. VaL), including 144 in the positive ion mode and 112 in the negative ion mode. A total of 177 different metabolites were screened from the comparison group between the blind calf aud its mother ( VaS. vs. CS), including 108 in the positive ion mode aud 69 in the negative ion mode. The content of rhodopsin in the blind calf was significantly lower than that of its mother, with log2 FC reaching - 2. 87. Compared with its mother, there were 30 differential metabolic pathways with P < 0. 05 in total in blind calves, and 10 differential metabolic pathways with corrected P < 0. 05 in total. Among them, bile secretion metabolic pathway had the largest distribution of differential metabolites. Compared with its mother, 4 metabolites in blind calves were significantly up-regulated, and 9 metabolites were significantly down-regulated. Compared with normal calves, there were 12 differential metabolic pathways with P <0. 05 in total in blind calves, and 16 differential metabolic pathways with corrected P < 0. 05 in total. Among them, bile secretion metabolic pathway distributed the most differential metabolites. Compared with normal calves, there were 5 metabolites significantly up-regulated and 4 metabolites significantly down-regulated in blind calves. [ Conclusion] The bile secretion metabolic pathway of blind calves is significantly different from that of their mothers and normal calves. The research suggests that the blindness of calves may be a disease of the body living in the liver, affecting the normal secretion of bile, leading to that the normal intake of fat-soluble vitamin A can not be absorbed and utilized, and thus affecting the vision of calves. In addition, compared with their mothers, the content of rhodopsin, which affects the cascade reaction of light transduction, is significantly down-regulated under the condition that there is no significant difference in vitamin A levels in the body of blind calves. The study suggests that the mutation of rhodopsin gene (RHO) encoding rhodopsin protein and the lack of rhodopsin protein might be another reason for their blindness. [ABSTRACT FROM AUTHOR]