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Effects of early neonatal development and delayed feeding immediately post-hatch on the hepatic lipogenic program in broiler chicks

机译:新生儿早期发育和孵化后立即喂食延迟对肉鸡肝脏脂肪形成程序的影响

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The embryo to neonate transition is a critical period of development that has significant impact on broiler production. During this time important genetic programs governing metabolism and growth are established. The goal of this work was to study the effects of early post-hatch (PH) development and the time of initiation of feeding on activation of the genetic program regulating hepatic lipogenesis. A comparison of liver total RNA samples at hatch and 7days PH was performed using oligonucleotide-based (Affymetrix GeneChip?) chicken genome microarrays. During the first week PH there was significant up-regulation of key lipogenic genes including: ATP citrate lyase (ACL), malic enzyme (ME), fatty acid synthase (FAS), acetyl-CoA carboxylase alpha (ACCα), stearoyl-CoA desaturase-1 (SCD-1), sterol regulatory element binding protein-2 (SREBP-2) and thyroid hormone responsive spot 14α (Spot 14α) among others. These findings were confirmed using gene-specific RT-PCR assays. In a follow-up study, we investigated the effects of withholding feed for the first 48h PH (delayed feeding, DF) on lipogenic gene expression through 8days PH. Body weight gain was significantly depressed by DF. Plasma levels of the major metabolic hormones that regulate lipogenic gene expression (insulin, glucagon and T_3) changed significantly during PH development, but were largely unaffected by DF. Plasma glucose was significantly lower in the DF group at 24h PH but recovered thereafter. In general, DF inhibited the up-regulation of lipogenic genes until feeding was initiated. Delayed up-regulation was also observed for the lipogenic transcription factor genes, SREBP-1, SREBP-2 and peroxisome proliferator-activated receptor gamma (PPARγ), but not for carbohydrate response element binding protein (ChREB) or liver X receptor (LXR). Our results offer additional insight into the transcriptional programming of hepatic lipogenesis in response to the transition from high fat (yolk) to high carbohydrate (feed) nutrition that occurs during early PH development.
机译:胚胎到新生儿的过渡是发育的关键时期,对肉鸡的生产有重要影响。在这段时间内,建立了控制新陈代谢和生长的重要遗传程序。这项工作的目的是研究孵化后早期(PH)的发展和开始喂食的时间对调节肝脂肪形成的遗传程序的激活的影响。使用基于寡核苷酸的(Affymetrix GeneChip?)鸡基因组微阵列比较孵化和PH值7天时的肝脏总RNA样品。在PH的第一周,主要的致脂基因显着上调,包括:柠檬酸ATP裂解酶(ACL),苹果酸酶(ME),脂肪酸合酶(FAS),乙酰辅酶A羧化酶α(ACCα),硬脂酰辅酶A去饱和酶-1(SCD-1),固醇调节元件结合蛋白2(SREBP-2)和甲状腺激素反应性斑点14α(Spot14α)等。这些发现已通过基因特异性RT-PCR分析得到证实。在一项后续研究中,我们调查了第一个48h PH的扣留饲料(延迟喂食,DF)对PH持续8天的致脂基因表达的影响。 DF显着抑制了体重增加。在PH形成过程中,调节脂肪形成基因表达的主要代谢激素(胰岛素,胰高血糖素和T_3)的血浆水平发生了显着变化,但不受DF的影响。 DF组在24h PH时血浆葡萄糖显着降低,但此后恢复。通常,DF会抑制脂肪基因的上调,直到开始喂养为止。还观察到脂生性转录因子基因,SREBP-1,SREBP-2和过氧化物酶体增殖物激活的受体γ(PPARγ)的延迟上调,但没有观察到碳水化合物反应元件结合蛋白(ChREB)或肝X受体(LXR) 。我们的研究结果提供了对早期脂肪发育期间发生的从高脂肪(蛋黄)到高碳水化合物(饲料)营养转变的肝脏脂肪生成转录程序的进一步了解。

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