关键词: broiler guanidinoacetic acid heat stress intestinal histomorphology mucosal barrier

Mesh : Male Animals Dietary Supplements Chickens Interleukin-1beta Tumor Necrosis Factor-alpha Diet / veterinary Heat-Shock Response Immunoglobulin A Animal Feed / analysis

来  源:   DOI:10.1093/jas/skac355   PDF(Pubmed)

Abstract:
The current study is designed to investigate dietary guanidinoacetic acid (GAA) supplementation on the growth performance, intestinal histomorphology, and jejunum mucosal barrier function of broilers that are subjected to chronic heat stress (HS). A total of 192 male broilers (28-d old) were randomly allocated to four groups. A chronic HS model (at a temperature of 32 °C and 50%-60% relative humidity for 24 h daily) was applied in the experiment. Normal control (NC, ad libitum feeding, 22 °C), HS group (HS, ad libitum feeding, 32 °C), pair-fed group (PF, received food equivalent to that consumed by the HS group on the previous day, 22 °C), guanidinoacetic acid group (HG, ad libitum feeding, supplementing the basal diet with 0.6 g/kg GAA, 32 °C). The experiment lasted from 28 to 35 and 28 to 42 d of age of broilers. Our results showed that broilers subjected to HS had lower average daily feed intake and average daily gain (P < 0.05), higher feed-to-gain ratio and relative length of the small intestine (P < 0.05), as well as lower relative weight and weight per unit length of the small intestine (P < 0.05). HS damaged the small intestinal histomorphology by decreasing the small intestinal VH and the VH/CD (P < 0.05). Compared with the HS group, supplementation with 0.6 g/kg GAA increased jejunal VH and VH/CD (P < 0.05), but decreased relative weight and relative length of the small intestine (P < 0.05). Moreover, in comparison with NC, HS elevated intestinal permeability (D-Lactic acid concentration and diamine oxidase activity) and mRNA expression levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α (P < 0.05), reduced jejunal mucus thickness, number of goblet cells, IgA + cell density, and mucin2 mRNA expression level of broilers (P < 0.05). Compared with the HS group, dietary GAA elevated jejunal mucus thickness, goblet cell number and IgA+ cell density (P < 0.05), and up-regulated jejunal mRNA expression of interleukin-1β and tumor necrosis factor-α (P < 0.05). In conclusion, HS impaired growth performance, and the intestinal mucosal barrier function of broilers. Dietary supplementation with 0.6 g/kg GAA alleviated HS-induced histomorphology changes of small intestine and jejunal mucosal barrier dysfunction.
With the global warming getting worse, heat stress (HS) has been a serious problem faced by poultry industry. As one of the main target organs, the intestine is easily affected by HS. Broilers are particularly sensitive to hot temperatures, and HS occurs when temperatures rise above the optimum (16–26 °C). Moreover, ambient humidity below 40% and above 80% also affects broilers adversely. HS can impair intestinal morphology and function of the intestinal barrier. The intestinal mucosal barrier not only plays key roles in nutrient digestion and absorption but also serves as the innate defense barrier fending off noxious substances within the intestinal luminal environment. Therefore, protecting intestinal mucosal barrier from HS is important to animal health. Nutrient regulation is an economical and effective method to alleviate HS of intensively-farmed broiler chickens. The results of current study demonstrated that chronic HS impaired the growth performance and intestinal mucosal barrier function of broilers, while dietary supplementation with 0.6 g/kg guanidinoacetic acid improved intestinal histomorphology and alleviated intestinal barrier dysfunction of broilers subjected to chronic HS, which is beneficial for improving health of broilers.
摘要:
本研究旨在探讨日粮中添加胍基乙酸(GAA)对生长性能的影响,肠道组织形态学,和经受慢性热应激(HS)的肉鸡的空肠粘膜屏障功能。将总共192只雄性肉鸡(28日龄)随机分为四组。在实验中应用慢性HS模型(在32°C的温度和50%-60%的相对湿度下,每天24小时)。正常控制(NC,随意喂食,22°C),HS组(HS,随意喂食,32°C),成对喂养组(PF,收到的食物相当于前一天HS组消耗的食物,22°C),胍基乙酸基团(HG,随意喂食,补充基础日粮0.6g/kgGAA,32°C)。实验持续28~35日龄和28~42日龄肉鸡。我们的结果表明,饲喂HS的肉鸡平均日采食量和平均日增重较低(P<0.05)。较高的饲料增重比和小肠的相对长度(P<0.05),以及较低的相对重量和单位长度的小肠重量(P<0.05)。HS通过降低小肠VH和VH/CD损害小肠组织形态学(P<0.05)。与HS组相比,补充0.6g/kgGAA可增加空肠VH和VH/CD(P<0.05),但小肠的相对重量和相对长度降低(P<0.05)。此外,与NC相比,HS提高肠通透性(D-乳酸浓度和二胺氧化酶活性)和白细胞介素-1β的mRNA表达水平,白细胞介素-6和肿瘤坏死因子-α(P<0.05),空肠粘液厚度减少,杯状细胞的数量,IgA+细胞密度,肉仔鸡黏蛋白2mRNA表达水平(P<0.05)。与HS组相比,膳食GAA升高空肠粘液厚度,杯状细胞数和IgA+细胞密度(P<0.05),空肠白细胞介素-1β和肿瘤坏死因子-αmRNA表达上调(P<0.05)。总之,HS增长业绩受损,对肉仔鸡肠黏膜屏障功能的影响。日粮补充0.6g/kgGAA可减轻HS诱导的小肠和空肠粘膜屏障功能障碍的组织形态学改变。
随着全球变暖的加剧,热应激(HS)一直是家禽业面临的严重问题。作为主要靶器官之一,肠道很容易受到HS的影响。肉鸡对高温特别敏感,当温度上升到最佳值(16-26°C)以上时,就会发生HS。此外,低于40%和高于80%的环境湿度也会对肉鸡产生不利影响。HS可以损害肠的形态和肠屏障的功能。肠粘膜屏障不仅在营养物质的消化和吸收中起关键作用,而且还作为抵御肠道环境中有毒物质的先天防御屏障。因此,保护肠粘膜屏障免受HS侵害对动物健康具有重要意义。营养调控是缓解集约化肉鸡HS的经济有效方法。目前的研究结果表明,慢性HS损害了肉鸡的生长性能和肠黏膜屏障功能,饲料中添加0.6g/kg胍基乙酸可改善慢性HS肉鸡的肠道组织形态,减轻肠屏障功能障碍,有利于提高肉鸡的健康水平。
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