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外源性胰岛素促进鸡胸肌中转录因子 B 细胞易位基因 1 和 2 的表达。

Exogenous insulin promotes the expression of B-cell translocation gene 1 and 2 in chicken pectoralis.

机构信息

College of Animal Science and Technology, Henan Agricultural University, Zhengzhou 450000, China.

College of Animal Science and Technology, Henan Agricultural University, Zhengzhou 450000, China.

出版信息

Poult Sci. 2022 Jul;101(7):101875. doi: 10.1016/j.psj.2022.101875. Epub 2022 Mar 25.

DOI:10.1016/j.psj.2022.101875
PMID:35544956
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9118148/
Abstract

B-cell translocation genes (BTG) have been proved to play important roles in carbohydrate metabolism through modifying insulin homeostasis and glucose metabolism. This study, therefore, was conducted to investigate the effects of exogenous insulin on the expression of BTG1 and BTG2 in chickens. Twenty-four-day-old broilers and layers were fasted for 16 h and randomly assigned to insulin treatment group (subcutaneously injected with 5 IU/kg body weight) or control group (received an equivalent volume of phosphate-buffered saline). Blood glucose concentration was measured, and it showed that the blood glucose concentrations in the layers were significantly (P < 0.05) higher than that in the broilers under fasting state. Response to exogenous insulin, the blood glucose concentrations were greatly reduced in both breeds. Of note, the blood glucose concentration restored to 62% of the basal state at 240 min (P < 0.05) after insulin stimulation in layers, whereas it was still in low level until 240 min in broilers (under fast state). Tissue profiling revealed that both BTG1 and BTG2 were abundantly expressed in the skeletal muscles of broilers. A negative correlation was observed between blood glucose and BTG1 (ρ = -0.289, P = 0.031) /BTG2 (ρ = -0.500, P < 0.001) in pectoralis, and BTG1 (ρ = -0.462, P < 0.001) in pancreas. As blood glucose decreased due to exogenous insulin administration (under fast state), the expression of both BTG1 and BTG2 notably upregulated in birds' pectoralis at 120 min and/or 240 min, meanwhile pancreas BTG1 was also upregulated. Re-feeding at 120 min elevated the blood glucose and reduced the expression of BTG genes in pectoralis generally. In addition, the change of BTG1 and BTG2 expression showed distinct difference between layers and broilers at 120 min and 240 min after insulin stimulation in pectoralis, pancreas and heart tissue; even after re-feeding at 120 min, BTG2 expression at 240 min after insulin injection was downregulated in the pectoralis of layers, while it was upregulated in that broilers. Collectively, these results indicated that response to exogenous insulin, chicken blood glucose exhibited breed-specific dynamic change, and meanwhile the expressions of both BTG1 and BTG2 genes in chickens were significantly altered by exogenous insulin in a breed- and tissue-specific manner. BTG1 and BTG2 genes may negatively regulate bird's blood glucose by promoting the glucose uptake corporately in pectoralis, and through regulating the insulin secretion in pancreas (especially BTG1).

摘要

B 细胞易位基因 (BTG) 已被证明通过调节胰岛素稳态和葡萄糖代谢在碳水化合物代谢中发挥重要作用。因此,本研究旨在研究外源性胰岛素对鸡 BTG1 和 BTG2 表达的影响。将 24 日龄的肉鸡和蛋鸡禁食 16 小时,并随机分配到胰岛素处理组(皮下注射 5IU/kg 体重)或对照组(接受等量的磷酸盐缓冲盐水)。测量血糖浓度,结果表明,禁食状态下蛋鸡的血糖浓度明显高于肉鸡(P < 0.05)。对外源性胰岛素的反应,两种品种的血糖浓度均显著降低。值得注意的是,在胰岛素刺激后 240 分钟,蛋鸡的血糖浓度恢复到基础状态的 62%(P < 0.05),而肉鸡在 240 分钟时仍处于低水平(在禁食状态下)。组织分析表明,BTG1 和 BTG2 在肉鸡的骨骼肌中均大量表达。在胸肌中,血糖与 BTG1(ρ= -0.289,P = 0.031)/BTG2(ρ= -0.500,P < 0.001)之间存在负相关,在胰腺中 BTG1(ρ= -0.462,P < 0.001)之间存在负相关。由于外源性胰岛素的给药导致血糖降低(在禁食状态下),在 120 分钟和/或 240 分钟时,鸟类胸肌中的 BTG1 和 BTG2 表达显著上调,同时胰腺 BTG1 也上调。120 分钟重新喂养通常会升高血糖并降低胸肌中 BTG 基因的表达。此外,在胰岛素刺激后 120 分钟和 240 分钟,BTG1 和 BTG2 表达的变化在胸肌、胰腺和心脏组织中在蛋鸡和肉鸡之间表现出明显的差异;即使在 120 分钟重新喂养后,蛋鸡在胰岛素注射后 240 分钟胸肌中的 BTG2 表达下调,而肉鸡则上调。总之,这些结果表明,对外源性胰岛素的反应,鸡的血糖表现出特定品种的动态变化,同时 BTG1 和 BTG2 基因在鸡中的表达也以品种和组织特异性的方式显著受到外源性胰岛素的调节。BTG1 和 BTG2 基因可能通过共同促进胸肌中的葡萄糖摄取来负调控鸟类的血糖,通过调节胰腺中的胰岛素分泌(尤其是 BTG1)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/cff95ba551f2/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/84f7fd520d09/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/b986ee668f0f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/0e0fc0315d9a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/2025464fe948/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/cff95ba551f2/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/84f7fd520d09/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/b986ee668f0f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/0e0fc0315d9a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/2025464fe948/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497b/9118148/cff95ba551f2/gr5.jpg

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