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下丘脑调控鸡摄食的外源性内脏脂肪素诱导的比较转录组分析。

Comparative transcriptome analysis of hypothalamus-regulated feed intake induced by exogenous visfatin in chicks.

机构信息

College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450002, China.

出版信息

BMC Genomics. 2018 Apr 11;19(1):249. doi: 10.1186/s12864-018-4644-7.

DOI:10.1186/s12864-018-4644-7
PMID:29642854
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5896085/
Abstract

BACKGROUND

The intracerebroventricular injection of visfatin increases feed intake. However, little is known about the molecular mechanism in chicks. This study was conducted to assess the effect of visfatin on the feeding behavior of chicks and the associated molecular mechanism.

RESULTS

In response to the intraventricular injection of 40 ng and 400 ng visfatin, feed intake in chicks was significantly increased, and the concentrations of glucose, insulin, TG, HDL and LDL were significantly altered. Using RNA-seq, we identified DEGs in the chick hypothalamus at 60 min after injection with various doses of visfatin. In total, 325, 85 and 519 DEGs were identified in the treated chick hypothalamus in the LT vs C, HT vs C and LT vs HT comparisons, respectively. The changes in the expression profiles of DEGs, GO functional categories, KEGG pathways, and PPI networks by visfatin-mediated regulation of feed intake were analyzed. The DEGs were grouped into 8 clusters based on their expression patterns via K-mean clustering; there were 14 appetite-related DEGs enriched in the hormone activity GO term. The neuroactive ligand-receptor interaction pathway was the key pathway affected by visfatin. The PPI analysis of DEGs showed that POMC was a hub gene that interacted with the maximum number of nodes and ingestion-related pathways, including POMC, CRH, AgRP, NPY, TRH, VIP, NPYL, CGA and TSHB.

CONCLUSION

These common DEGs were enriched in the hormone activity GO term and the neuroactive ligand-receptor interaction pathway. Therefore, visfatin causes hyperphagia via the POMC/CRH and NPY/AgRP signaling pathways. These results provide valuable information about the molecular mechanisms of the regulation of food intake by visfatin.

摘要

背景

脑室内注射内脂素可增加摄食量。然而,目前对于禽类,人们对此知之甚少。本研究旨在评估内脂素对禽类摄食行为的影响及其相关的分子机制。

结果

脑室注射 40ng 和 400ng 内脂素后,雏鸡的采食量明显增加,血糖、胰岛素、甘油三酯、高密度脂蛋白和低密度脂蛋白浓度也明显改变。用 RNA-seq 技术,我们在脑室注射不同剂量内脂素 60min 后,鉴定出雏鸡下丘脑的差异表达基因。与对照组相比,处理组中分别有 325 个、85 个和 519 个差异表达基因在 LT 与 C、HT 与 C 和 LT 与 HT 比较中被鉴定。通过内脂素介导的摄食调节,分析了差异表达基因的表达谱、GO 功能分类、KEGG 通路和 PPI 网络的变化。通过 K-均值聚类,根据差异表达基因的表达模式将其分为 8 个簇;在激素活性 GO 术语中富集了 14 个与食欲相关的差异表达基因。神经活性配体-受体相互作用途径是受内脂素影响的关键途径。差异表达基因的 PPI 分析表明,POMC 是一个与最大数量节点相互作用的枢纽基因,与摄食相关的途径包括 POMC、CRH、AgRP、NPY、TRH、VIP、NPYL、CGA 和 TSHB。

结论

这些共同的差异表达基因富集在激素活性 GO 术语和神经活性配体-受体相互作用途径中。因此,内脂素通过 POMC/CRH 和 NPY/AgRP 信号通路引起摄食过度。这些结果为内脂素调节食物摄入的分子机制提供了有价值的信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/baeef978bec7/12864_2018_4644_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/f4ab9e9c82d4/12864_2018_4644_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/cd4bbe1c227f/12864_2018_4644_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/acda49a7f435/12864_2018_4644_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/18bde22558d0/12864_2018_4644_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/a7c6e6a7b394/12864_2018_4644_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/115705ba87fd/12864_2018_4644_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/ef22de666aff/12864_2018_4644_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/093eda21ed51/12864_2018_4644_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/baeef978bec7/12864_2018_4644_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/f4ab9e9c82d4/12864_2018_4644_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/cd4bbe1c227f/12864_2018_4644_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/acda49a7f435/12864_2018_4644_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/18bde22558d0/12864_2018_4644_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/a7c6e6a7b394/12864_2018_4644_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/115705ba87fd/12864_2018_4644_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/ef22de666aff/12864_2018_4644_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/093eda21ed51/12864_2018_4644_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9d/5896085/baeef978bec7/12864_2018_4644_Fig9_HTML.jpg

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