Effects of riboflavin deficiency on the lipid metabolism of duck breeders and duck embryos.
Effects of riboflavin deficiency on the lipid metabolism of duck breeders and duck embryos.
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DOI：
10.1016/j.psj.2021.101342
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发表时间：
2021-10
期刊：
影响因子：
4.4
通讯作者：
Hou SS
中科院分区：
文献类型：
--
作者：
Zhang B;Tang J;Wu YB;Cao JT;Xing GN;Sun PX;Huang W;Xie M;Hou SS
本试验旨在探讨饲粮核黄素缺乏（RD）对种鸭及鸭胚脂质代谢的影响。选取40周龄北京白鸭母鸭40只，随机分为2组，分别饲喂RD饲粮（1.48 mg核黄素/kg， CON）和对照组饲粮（16.48 mg核黄素/kg， CON），试验期14周。每组20只种鸭（每组10个重复，每个重复2只），试验鸟均为单笼饲养。试验结束时，测定种鸭和鸭胚的繁殖性能、肝核黄素、肝黄素单核苷酸（FMN）、肝黄素腺嘌呤二核苷酸（FAD）、肝脏形态、肝脏脂质含量和肝脏蛋白表达。结果表明，与对照组相比，RD对产蛋率和蛋育性无显著影响，但降低了蛋的孵化率、鸭胚重、肝核黄素、FMN和FAD水平（均P < 0.05）。RD鸭肝脏脂滴增大，总脂、甘油三酯和游离脂肪酸积累过多（均P < 0.05）。除脂质过度积累外，中链特异性酰基辅酶a脱氢酶表达下调（P < 0.05），短链特异性酰基辅酶a脱氢酶表达上调（P < 0.05）。RD不影响母鸭肝脏酰基辅酶a脱氢酶家族成员9 （ACAD9）的表达，但RD组鸭胚胎肝脏ACAD9的表达降低（P < 0.05）。总之，饲粮中添加RD降低了蛋的孵化率，抑制了鸭胚的发育。由于黄素蛋白表达减少，导致肝脏脂质利用受到抑制，母体和胚胎的脂质积累增加受到损害。上述结果提示，RD引起的鸭胚发育异常和低孵化率可能与母体及胚胎脂质代谢紊乱有关。
This study aimed to evaluate the effects of dietary riboflavin deficiency (RD) on the lipid metabolism of duck breeders and duck embryos. A total of 40 female 40-wk-old white Pekin duck breeders were randomly divided into 2 groups, received either RD diet (1.48 mg riboflavin/kg) or control diet (16.48 mg riboflavin/kg, CON) for 14 wk. Each group consisted of 20 duck breeders (10 replicates per group, 2 birds per replicate), and all experiment birds were single-caged. At the end of the experiment, reproductive performance, hepatic riboflavin, hepatic flavin mononucleotide (FMN), hepatic flavin adenine dinucleotide (FAD), hepatic morphology, hepatic lipid contents, and hepatic protein expression of duck breeders and duck embryos were measured. The results showed that the RD had no effect on egg production and egg fertility but reduced egg hatchability, duck embryo weight, hepatic riboflavin, FMN, and FAD status compared to results obtained in the CON group (all P < 0.05). Livers from RD ducks presented enlarged lipid droplets, excessive accumulation of total lipids, triglycerides, and free fatty acids (all P < 0.05). In addition to excessive lipids accumulation, medium-chain specific acyl-CoA dehydrogenase expression was downregulated (P < 0.05), and short-chain specific acyl-CoA dehydrogenase expression was upregulated in maternal and embryonic livers (P < 0.05). RD did not affect maternal hepatic acyl-CoA dehydrogenase family member 9 (ACAD9) expression, but duck embryonic hepatic ACAD9 expression was reduced in the RD group (P < 0.05). Collectively, dietary RD conditioned lower egg hatchability and inhibited the development of duck embryos. Increased accumulation of lipids, both maternal and embryo, was impaired due to the reduced flavin protein expression, which caused inhibition of hepatic lipids utilization. These findings suggest that abnormal duck embryonic growth and low hatchability caused by RD might be associated with disorders of lipid metabolism in maternal as well as embryos.
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DOI：
10.1016/0305-0491(94)00247-r
发表时间：
1995-06-01
影响因子：
2.2
作者：
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