Integrating RNA-sequencing and untargeted LC-MS metabolomics to evaluate the effect of lysine deficiency on hepatic functions in Holstein calves
文献类型: 外文期刊
第一作者: Kong, Fanlin
作者: Kong, Fanlin;Bi, Yanliang;Cui, Kai;Li, Yuan;Diao, Qiyu;Tu, Yan;Wang, Bing;Fu, Tong
作者机构:
关键词: Lysine deficiency; Holstein calves; Liver; Lipid metabolism
期刊名称:AMINO ACIDS ( 影响因子:3.52; 五年影响因子:3.6 )
ISSN: 0939-4451
年卷期: 2020 年 52 卷 5 期
页码:
收录情况: SCI
摘要: Lysine (Lys) is majorly metabolized in the liver. The liver functional consequences of a dietary Lys deficiency in young Holstein calves are unknown. This study aimed to investigate the effects of Lys deficiency in Holstein calf livers using RNA-sequencing and untargeted LC-MS metabolomics. Calves (n = 36; initial body weight 101.2 +/- 10.8 kg; 90-day-old) were fed restricted diets, for 90 days, containing 19.2% crude protein that varied in Lys content (PC group 1.21%; PC-Lys group 0.85%; dry matter basis) for 90 days. Body weight, average daily gain, gain/feed, and Lys intake were significantly decreased in response to Lys deficiency (P < 0.05). Dry matter intake was not altered (P > 0.05). Network and pathway analyses revealed that noradrenaline, adenosine 5 '-monophosphate, acetyl-CoA, and coenzyme A were significantly decreased. Regulating of lipolysis in adipocytes pathway and fatty acid degradation pathway were downregulated. We also identified eight significantly differentially expressed genes (SDEGs), among which adrenoceptor beta 2 (ADRB2), WAP four-disulfide core domain 2 (WFDC2), and claudin-4 (CLDN4) were associated with inhibition of lipolysis, and carbon catabolite repression 4-like (CCRN4L), FOS like 2 (FOSL2), and arginase 2 (ARG2) were associated with inhibiting lipid synthesis. Correlation tests showed that coenzyme A was strongly correlated with SDEGs (0.82 <=|r|<= 0.96). Acetyl-CoA and adenosine 5 '-monophosphate were strongly correlated with CCRN4L (0.90 <=|r|<= 0.92), indicating a strong correlation between the changes in SDEGs and these metabolites. In conclusion, Lys deficiency caused dysplasia and affected lipid metabolism in the liver by inhibiting lipolysis and lipid synthesis in calves.
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