Dietary methionine deficiency stunts growth and increases fat deposition via suppression of fatty acids transportation and hepatic catabolism in Pekin ducks

文献类型： 外文期刊

第一作者： Wu, Yongbao

作者： Wu, Yongbao;Tang, Jing;Zhang, Bo;Cao, Junting;Guo, Zhanbao;Xie, Ming;Zhou, Zhengkui;Hou, Shuisheng;Wu, Yongbao;Wen, Zhiguo;Cao, Junting;Zhao, Lulu

作者机构：

关键词： Fat deposition; Hepatic catabolism; Methionine deficiency; Pekin duck; Proteomics

期刊名称：JOURNAL OF ANIMAL SCIENCE AND BIOTECHNOLOGY （ 影响因子：6.175； 五年影响因子：6.853 ）

ISSN： 1674-9782

年卷期： 2022 年 13 卷 1 期

页码：

收录情况： SCI

摘要： Background Although methionine (Met), the first-limiting dietary amino acid, has crucial roles in growth and regulation of lipid metabolism in ducks, mechanisms underlying are not well understood. Therefore, the objective was to use dietary Met deficiency to investigate the involvement of Met in lipid metabolism and fat accumulation of Pekin ducks. Methods A total of 150 male Pekin ducks (15-d-old, 558.5 +/- 4.4 g) were allocated into 5 groups (6 replicates with 5 birds each) and fed corn and soybean meal-based diets containing 0.28%, 0.35%, 0.43%, 0.50%, and 0.58% Met, respectively, for 4 weeks. Met-deficient (Met-D, 0.28% Met) and Met-adequate (Met-A, 0.43% Met) groups were selected for subsequent molecular studies. Serum, liver, and abdominal fat samples were collected to assess the genes and proteins involved in lipid metabolism of Pekin ducks and hepatocytes were cultured in vivo for verification. Results Dietary Met deficiency caused growth depression and excess fat deposition that were ameliorated by feeding diets with adequate Met. Serum triglyceride and non-esterified fatty acid concentrations increased (P < 0.05), whereas serum concentrations of total cholesterol, low density lipoprotein cholesterol, total protein, and albumin decreased (P < 0.05) in Met-D ducks compared to those in Met-A ducks. Based on hepatic proteomics analyses, dietary Met deficiency suppressed expression of key proteins related to fatty acid transport, fatty acid oxidation, tricarboxylic acid cycle, glycolysis/gluconeogenesis, ketogenesis, and electron transport chain; selected key proteins had similar expression patterns verified by qRT-PCR and Western blotting, which indicated these processes were likely impaired. In vitro verification with hepatocyte models confirmed albumin expression was diminished by Met deficiency. Additionally, in abdominal fat, dietary Met deficiency increased adipocyte diameter and area (P < 0.05), and down-regulated (P < 0.05) of lipolytic genes and proteins, suggesting Met deficiency may suppress lipolysis in adipocyte. Conclusion Taken together, these data demonstrated that dietary Met deficiency in Pekin ducks resulted in stunted growth and excess fat deposition, which may be related to suppression of fatty acids transportation and hepatic catabolism.

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