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日粮磷水平通过调节肉鸡肠道和下丘脑厌食基因的表达来调控食欲。

Dietary phosphorus level regulates appetite through modulation of gut and hypothalamic expression of anorexigenic genes in broiler chickens.

作者信息

Aderibigbe A S, Ajuwon K M, Adeola O

机构信息

Department of Animal Sciences, Purdue University, West Lafayette, IN 47907, USA.

Department of Animal Sciences, Purdue University, West Lafayette, IN 47907, USA.

出版信息

Poult Sci. 2022 Feb;101(2):101591. doi: 10.1016/j.psj.2021.101591. Epub 2021 Nov 9.

Abstract

Two experiments were designed to elucidate gut and hypothalamic molecular regulation of appetite by dietary phosphorus (P) concentration in broiler chickens. Birds (192 Cobb-500 broiler chickens) were randomly assigned to 3 experimental diets in experiment 1 (Exp. 1) and 24 broiler chickens were randomly assigned to 3 treatment groups in Exp. 2. Each diet comprised 8 replicate cages, with either 8 birds (Exp. 1) or 1 bird (Exp. 2) per replicate cage. In Exp. 1, diets contained 1.2 (P-deficient), 2.8 (P-marginal) or 4.4 (P-adequate) g/kg non-phytate P (nPP). In Exp. 2, birds fed the P-adequate diet were pair-fed (PF) to the feed consumption levels of birds fed the P-deficient diet. Feed intake and BW gain (P < 0.001) decreased in birds fed the P-deficient diet in Exp. 1. Birds fed the P-deficient diet had similar feed intake and BW gain with PF group fed the P-adequate diet (Exp. 2) but was significantly lower (P < 0.001) than birds fed the P-adequate diets. Sodium-phosphate cotransporter (NaPi-IIb) mRNA was upregulated (P < 0.05) in both experiments. Conversely, cholecystokinin (CCK) mRNA was downregulated (P < 0.01) in birds fed P-deficient diets. Anorexia-related hypothalamic cholecystokinin receptor (CCKAR) and melanocortin receptors (MC3R and MC4R) were upregulated (P < 0.05) in birds fed P-deficient diets, in both experiments. The current data show that dietary P deficiency decreases feed intake in broiler chickens by altering the expression of anorexigenic genes in the gut and hypothalamus of broiler chickens.

摘要

设计了两个实验,以阐明日粮磷(P)浓度对肉鸡食欲的肠道和下丘脑分子调控。在实验1中,将192只科宝500肉鸡随机分配到3种实验日粮中,在实验2中,将24只肉鸡随机分配到3个处理组。每种日粮包含8个重复笼,每个重复笼中有8只鸡(实验1)或1只鸡(实验2)。在实验1中,日粮含有1.2(缺磷)、2.8(边缘磷)或4.4(磷充足)g/kg非植酸磷(nPP)。在实验2中,给采食磷充足日粮的鸡进行配对饲喂(PF),使其采食水平与采食缺磷日粮的鸡相同。在实验1中,采食缺磷日粮的鸡的采食量和体重增加量(P<0.001)下降。采食缺磷日粮的鸡与采食磷充足日粮的PF组的采食量和体重增加量相似(实验2),但显著低于采食磷充足日粮的鸡(P<0.001)。在两个实验中,磷酸钠共转运体(NaPi-IIb)mRNA均上调(P<0.05)。相反,采食缺磷日粮的鸡的胆囊收缩素(CCK)mRNA下调(P<0.01)。在两个实验中,采食缺磷日粮的鸡的厌食相关下丘脑胆囊收缩素受体(CCKAR)和黑皮质素受体(MC3R和MC4R)均上调(P<0.05)。当前数据表明,日粮缺磷通过改变肉鸡肠道和下丘脑厌食基因的表达来降低肉鸡的采食量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/493f/8665405/251dfd910384/gr1.jpg

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