Protein and Amino Acid Metabolism in Poultry during and after Heat Stress: A Review

✅ 全文

家禽热应激期间及之后的蛋白质与氨基酸代谢:综述

作者 Mohammed M. Qaid; Maged A. Al‐Garadi 期刊 Animals 发表日期 2021 ISSN 2076-2615 DOI 10.3390/ani11041167 类型 原创研究 (Original Research)

📄 中文摘要 Chinese Abstract

中文
热应激是现代家禽生产中的主要环境挑战,特别是在热带和亚热带地区,高温环境会损害肉鸡的生产性能。现代商品肉鸡由于其快速生长和高代谢产热,特别容易受到影响,这会损害其体温调节能力。热应激导致采食量减少、营养代谢改变以及重大经济损失。除了采食量下降外,热应激还会独立地干扰蛋白质和氨基酸(AA)代谢,影响肌肉沉积和整体生长。本综述综合了当前关于热应激下蛋白质和氨基酸代谢的知识,考察了生理和激素反应,并评估了营养策略——特别是氨基酸补充——以减轻这些影响并增强肉鸡的耐热性。

📋 英文结构化总结 English Structured Summary

全文整理

EN

Background:

Heat stress is a major environmental challenge in modern poultry production, particularly in tropical and subtropical regions where high ambient temperatures impair broiler performance. Modern commercial broilers are especially susceptible due to their rapid growth rates and high metabolic heat production, which compromise thermoregulation. Heat stress leads to reduced feed intake, altered nutrient metabolism, and significant economic losses. Beyond decreased consumption, heat stress independently disrupts protein and amino acid (AA) metabolism, affecting muscle deposition and overall growth. This review synthesizes current knowledge on protein and AA metabolism under heat stress, examines physiological and hormonal responses, and evaluates nutritional strategies—particularly AA supplementation—to mitigate these effects and enhance thermotolerance in broilers.

Methods:

N/A – Review article

Results:

Heat stress negatively impacts protein metabolism by reducing protein synthesis and increasing catabolism, leading to lower nitrogen retention and muscle protein deposition. Chronic heat exposure decreases plasma free amino acid concentrations—especially branched-chain and sulfur-containing AAs—while elevating glutamic acid, aspartic acid, and phenylalanine. Blood urea nitrogen (BUN) and uric acid levels rise initially due to muscle breakdown but may normalize over time. Heat shock proteins (HSPs), particularly HSP70, are upregulated during stress and play protective roles, with glutamine shown to enhance HSP expression and reduce protein degradation. Hormonally, corticosterone promotes proteolysis and gluconeogenesis from AA carbon skeletons, while insulin’s anabolic effects are diminished. Nutritional interventions such as balanced AA profiles, glutamine supplementation, and optimized dietary protein levels have demonstrated potential to alleviate heat stress effects.

Data Summary:

Studies indicate that increasing dietary protein from 20% to 25% at 32 °C did not affect protein synthesis rates but improved muscle protein deposition, likely by reducing protein breakdown. Glutamine supplementation has been associated with improved growth performance and humoral immunity in heat-stressed broilers. Dietary adjustments reducing nitrogen excretion by 21% between 28 and 49 days of age have been reported under high-temperature conditions. Broilers exposed to chronic heat stress show decreased feed intake, lower body weight gain, and reduced breast meat yield, with AA digestibility and retention significantly impaired.

Conclusions:

High ambient temperatures reduce dietary amino acid intake and disrupt protein metabolism in broilers, resulting in decreased protein accretion and growth. While reduced feed intake contributes to production losses, direct metabolic and endocrine alterations under heat stress play an independent and significant role. Amino acid supplementation—especially functional AAs like glutamine, leucine, and arginine—offers a promising strategy to support thermotolerance and maintain performance. However, optimal AA requirements under heat stress remain unclear, and further research is needed to define ideal amino acid ratios in warm climates. Additionally, emerging genetic tools may enable breeding for improved heat resilience in poultry.

Practical Significance:

This review provides actionable insights for poultry producers and nutritionists to mitigate heat stress through targeted dietary strategies, including precise amino acid balancing, supplementation with functional amino acids (e.g., glutamine), and careful management of dietary protein levels to avoid excessive heat increment. These approaches can help maintain broiler growth, health, and welfare under high-temperature conditions, supporting sustainable poultry production in warming climates.

📋 中文结构化总结 Chinese Structured Summary

中文

背景:

热应激是现代家禽生产中的主要环境挑战,特别是在热带和亚热带地区,高温环境会损害肉鸡的生产性能。现代商品肉鸡由于其快速生长和高代谢产热,特别容易受到影响,这会损害其体温调节能力。热应激导致采食量减少、营养代谢改变以及重大经济损失。除了采食量下降外,热应激还会独立地干扰蛋白质和氨基酸(AA)代谢,影响肌肉沉积和整体生长。本综述综合了当前关于热应激下蛋白质和氨基酸代谢的知识,考察了生理和激素反应,并评估了营养策略——特别是氨基酸补充——以减轻这些影响并增强肉鸡的耐热性。

方法:

不适用——综述文章

结果:

热应激通过减少蛋白质合成和增加分解代谢对蛋白质代谢产生负面影响,导致氮保留和肌肉蛋白沉积降低。慢性热暴露会降低血浆游离氨基酸浓度——特别是支链氨基酸和含硫氨基酸——同时升高谷氨酸、天冬氨酸和苯丙氨酸水平。血尿素氮(BUN)和尿酸水平最初因肌肉分解而升高,但可能随时间恢复正常。热休克蛋白(HSPs),特别是HSP70,在应激期间上调并发挥保护作用,谷氨酰胺被证明可增强HSP表达并减少蛋白质降解。在激素方面,皮质酮促进蛋白质分解和氨基酸碳骨架的糖异生,而胰岛素的合成代谢作用减弱。平衡氨基酸谱、谷氨酰胺补充和优化日粮蛋白质水平等营养干预措施已显示出缓解热应激效果的潜力。

数据总结:

研究表明,在32°C条件下将日粮蛋白质从20%增加到25%并未影响蛋白质合成率,但改善了肌肉蛋白沉积,可能是通过减少蛋白质分解实现的。谷氨酰胺补充与热应激肉鸡生长性能和体液免疫的改善相关。据报道,在高温条件下,日粮调整在28至49日龄期间使氮排泄减少了21%。暴露于慢性热应激的肉鸡表现出采食量减少、体重增长降低和胸肉产量下降,氨基酸消化率和保留率显著受损。

结论:

高温环境降低了肉鸡的膳食氨基酸摄入并扰乱蛋白质代谢,导致蛋白质沉积和生长减少。虽然采食量减少导致了生产损失,但热应激下的直接代谢和内分泌改变起着独立且重要的作用。氨基酸补充——特别是谷氨酰胺、亮氨酸和精氨酸等功能性氨基酸——为支持耐热性和维持生产性能提供了有前景的策略。然而,热应激下的最佳氨基酸需求仍不明确,需要进一步研究以确定温暖气候下的理想氨基酸比例。此外,新兴的遗传工具可能使家禽耐热性育种成为可能。

实践意义:

本综述为家禽生产者和营养学家提供了可操作的见解,通过有针对性的饮食策略来缓解热应激,包括精确的氨基酸平衡、功能性氨基酸(如谷氨酰胺)的补充,以及日粮蛋白质水平的精细管理以避免过量的热增耗。这些方法可以帮助在高温条件下维持肉鸡的生长、健康和福利,支持气候变暖条件下的可持续家禽生产。

📖 英文全文 English Full Text

EN

Animals (Basel) Animals (Basel) 2763 animals animals Animals : an Open Access Journal from MDPI 2076-2615 Multidisciplinary Digital Publishing Institute (MDPI) PMC8074156 PMC8074156.1 8074156 8074156 33921616 10.3390/ani11041167 animals-11-01167 1 Review Protein and Amino Acid Metabolism in Poultry during and after Heat Stress: A Review https://orcid.org/0000-0003-0934-9690 Qaid Mohammed M. 1 2 * https://orcid.org/0000-0002-0388-7669 Al-Garadi Maged A. 1 2 * Morgan Natalie Academic Editor 1 Animal Production Department, College of Food and Agriculture Sciences, King Saud University, Riyadh 11451, Saudi Arabia 2 Veterinary Medicine Faculty, Thamar University, Dhamar 13020, Yemen * Correspondence: mqaid@ksu.edu.sa (M.M.Q.); malgaradi@ksu.edu.sa (M.A.A.-G.); Tel.: +966-509-844-024 (M.M.Q.); +966-533429411 (M.A.A.-G.) 19 4 2021 4 2021 11 4 380265 1167 11 3 2021 12 4 2021 19 04 2021 27 04 2021 17 05 2021 © 2021 by the authors. 2021 https://creativecommons.org/licenses/by/4.0/ Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/ ). Simple Summary Broilers must be reared under thermoneutral conditions and comfort zones; therefore, any deviation from the neutral thermal zone causes stress and a consequent disturbance in the turnover or the metabolism of nutrients. This review addressed the biosynthesis of amino acids and/or protein metabolism under normal conditions and heat stress conditions. In addition, hormonal responses to stress and the role of endocrine hormones in protein metabolism have been reviewed. In addition, the aim of this review is to summarize the studies related to the assessment of heat stress, the physiological stress regulation mechanism, and the nutritional strategies for the prevention of heat stress in poultry. Abstract This review examined the influence of environmental heat stress, a concern facing modern broiler producers, on protein metabolism and broiler performance, as well as the physiological mechanisms that activate and control or minimize the detrimental impacts of stress. In addition, available scientific papers that focused on amino acids (AA) digestibility under stress conditions were analyzed. Furthermore, AA supplementation, a good strategy to enhance broiler thermotolerance, amelioration, or stress control, by keeping stress at optimal levels rather than its elimination, plays an important role in the success of poultry breeding. Poultry maintain homeothermy, and their response to heat stress is mainly due to elevated ambient temperature and the failure of effective heat loss, which causes a considerable negative economic impact on the poultry industry worldwide. Reduced feed intake, typically observed during heat stress, was the primary driver for meat production loss. However, accumulating evidence indicates that heat stress influences poultry metabolism and endocrine profiles independently of reduced feed intake. In conclusion, high ambient temperatures significantly reduced dietary AA intake, which in turn reduced protein deposition and growth in broilers. Further studies are required to determine the quantity of the AA needed in warm and hot climates and to introduce genetic tools for animal breeding associated with the heat stress in chickens. amino acids broiler heat stress heat tolerance protein metabolism pmc-status-qastatus 0 pmc-status-live yes pmc-status-embargo no pmc-status-released yes pmc-prop-open-access yes pmc-prop-olf no pmc-prop-manuscript no pmc-prop-legally-suppressed no pmc-prop-has-pdf yes pmc-prop-has-supplement no pmc-prop-pdf-only no pmc-prop-suppress-copyright no pmc-prop-is-real-version no pmc-prop-is-scanned-article no pmc-prop-preprint no pmc-prop-in-epmc yes pmc-license-ref CC BY 1. Introduction Poultry meat is an essential source of dietary protein, and the industry has developed high grade poultry because of improved farming techniques, automation equipment, and comprehensive and balanced feeding, and other new technologies [ 1 ]. In the past decade, broiler production has increased rapidly in tropical and subtropical areas and is expected to sustain robust growth in the future. However, according to a review [ 2 ], high environmental temperatures are one of the greatest challenges of poultry and live stock performance, leading to the decline in production efficiency in these countries. Furthermore, modern commercial broilers are more sensitive to heat stress than previous generations due to their higher performance, growth rate, and feed conversion efficiency [ 3 ]. Indeed, commercial poultry strains can reach a high production yield, but their body metabolism, being comparatively accelerated, has poor thermoregulation and is poorly adapted to the living environments compared to native backyard chickens [ 1 ]. The higher growth rate of broilers has several consequences, such as higher feed consumption and metabolism and elevated production of internal heat. To reduce the heat load and avoid heat-induced mortality in birds, heat loss and/or lowering heat production could be achieved through reduced feed consumption, resulting in a depressed growth rate and lower final body weight, reduced breast meat weight, and lower egg quality, size, and rate in hens. In addition, the decreased feed consumption could result in nutrient deficiency, such as proteins, AA, and energy [ 4 , 5 , 6 ]. Among the environmental factors, heat stress negatively affects feed consumption, body weight gain [ 7 ], and carcass characteristics [ 2 ]. Additionally, HS may cause oxidative stress in the body and develop many free radicals, stimulating membrane lipid peroxidation, and hence the degradation of DNA and protein membranes [ 8 , 9 ]. In poultry, mitochondrial superoxide production as oxidative stress was observed on exposure to HS [ 9 ]. Besides the role of AA as protein and peptide components, some AA (e.g., glutamine, cysteine, leucine, arginine, tryptophan, and proline) are involved in the regulation of metabolic pathways, thereby affecting growth, protein accumulation, maintenance, immunity, and health [ 10 ]. The ambient temperature impacts the protein turnover rate in broiler skeletal muscle [ 11 ]. Not only protein anabolism, but also protein catabolism are energetically expensive. The growth depression of heat-exposed chickens showed lower protein gain and retention. High protein sources have beneficial effects through the improved growth of heat-stressed broilers [ 12 ]. They indicated that protein synthesis in broilers was more affected than protein breakdown with HS, resulting in reduced protein deposition in the skeletal muscles. A review [ 11 ] showed that the high ambient temperatures and dietary protein consumption affected muscle protein turnover in broilers. In broiler chickens, HS alters muscle protein and AA metabolism and accelerates liver gluconeogenesis for energy supply [ 13 ]. Dietary approaches, such as modifications of energy and protein content of the diet, are the most practical and preferred ways to alleviate heat distress in poultry and enhance broiler performance under these conditions [ 14 , 15 ]. Improving the overall equilibrium of the dietary AA was more effective than increasing total protein consumption [ 16 ]. Limited studies are available that address the effects of HS on protein metabolism in broilers. Therefore, it is necessary to detect mechanisms or methods that allow producers to effectively reduce the detrimental influences of environmental HS on broilers, in particular on protein metabolism via protein accretion or degradation of muscle. The present review will focus on the effects of environmental heat stress on protein metabolism and broiler performance, as well as the physiological mechanisms and nutritional strategies that mitigate the negative effects of heat stress, particularly the role of AA in reducing HS in stressed broilers. 2. Amino Acid and/or Protein Metabolism AA are required for most biological activities. The AA transport into the apical membrane and out of the lateral basal membrane of enterocytes. Their transport relies on sodium-dependent symporters, proton-motive forces, antiporters, and the gradient of other AA. The metabolic fate of absorbed AA mainly depends on nutrient availability [ 17 ]. AA moving through catabolic pathways ultimately serve as precursors of gluconeogenesis [ 13 ] and contribute to 40% of the total AA loss in fasted animals. Proteins are synthesized from free AA, which become available either from dietary (the end product of digestion) or from metabolic origins as the result of AA biosynthesis within the body. These AA, either circulating via the blood or accumulating within tissues, form pools. The AA concentrations within these pools are based on the equilibrium between gains and losses [ 18 ]. Dietary AA are used to build protein for muscle growth, membrane glycoproteins, and enzymes involved in numerous biochemical processes, and act as precursors for the synthesis of DNA/RNA [ 10 ]. The AA catabolize in the liver to integrate into protein, which supplies peripheral tissues [ 13 ]. Protein turnover refers to the equilibrium between the anabolism and catabolism of protein. The metabolic utilization of AA is equally diverse. Anabolism or protein synthesis facilitates dietary AA to fuse into proteins, or biosynthesize in the body tissues. Catabolism occurs through the breakdown of proteins to build amino groups that produce urea or further protein. In addition, to produces carbon skeleton molecules for glucose production (glucogenesis) or fatty acids (lipogenesis), carbon dioxide, and the release of energy. The role of endocrine hormones in protein metabolism is shown in Table 1 . Nitrogen excretion can be used to determine protein balance through the measurement of nitrogen losses during protein catabolism or recycling [ 18 ]. Endogenous or dietary proteins hydrolyze the previous absorption. The tissue proteins of birds are renewed frequently with the liberation of endogenous AA. Furthermore, there are many metabolic reactions converting metabolites into nonessential AA [ 18 ]. Recently, AA are applied not only as signaling molecules of the cell and the protein phosphorylation cascade, but also as regulators of gene expression. Moreover, AA are fundamental precursors for hormone synthesis and other nitrogenous elements that have considerable biological significance. Normal levels of AA and their metabolites, such as glutathione, polyamines, taurine, nitric oxide, serotonin, and thyroid hormones are needed for their functions. Nevertheless, elevated levels of AA and their metabolites, such as ammonia, asymmetric dimethylarginine, and homocysteine are considered pathogenic for the body, and lead to oxidative stress, and cause diseases and disorders of the cardiovascular and neurological systems. Therefore, an ideal balance of AA in the feed and bloodstream is crucial for the homeostasis of the body. AA not only have a role as the building blocks of polypeptides and proteins, but also regulate the fundamental metabolic routes that are essential for growth, maintenance, immunity, and reproduction. These functional AA include glutamine, leucine, proline, arginine, cysteine, and tryptophan [ 10 ]. 3. Biosynthesis of Amino Acids Birds and all vertebrates, dissimilar to plants and many bacteria, are unable to synthesize some AA, so these are termed essential AA and are required for tissue renewal through protein synthesis. Thus, essential AA must be supplemented in the diet. For protein synthesis, all AA are similarly essential owing to the absence of any AA interfere with the anabolic processes. However, nutritionally AA are classified into three groups [ 18 ]. Essential AA must be provided by feed and may be classified into two groups. One group is strictly essential because they cannot be synthesized, even from AA metabolic intermediates, such as glucogenic that yield intermediates of glycolysis pathway or ketogenic that yield intermediates of acetyl-CoA or acetoacetate. The transaminases of that group are absent, for instance methionine, lysine, tryptophan, threonine, and phenylalanine. The other group may be insufficiently synthesized from their precursors, for example, glycine, leucine, isoleucine, valine, arginine, histidine, and proline. Semiessential AA may be synthesized from essential AA. Tyrosine and cysteine originate from phenylalanine and methionine, respectively. Cysteine is synthesized from serine (nonessential AA) and methionine (essential AA). Nonessential AA are easily synthesized from intermediary metabolites or similarly nonessential AA: alanine, serine, aspartic and glutamic acids in the former group; and asparagine and glutamine in the latter group [ 18 ]. 4. Effect of HS on Protein Metabolism or Turnover Heat as a stress factor affects protein metabolism during the postabsorptive stage as muscle breakdown and changes in the quantity of lean tissue may occur in different species [ 21 ]. In the muscle protein, the RNA/DNA synthesis capacity is reduced by HS [ 22 ]. During environmental hyperthermia, muscle tissue catabolism is increased due to increased plasma markers during muscle breakdown. In lactating cows, HS increases plasma urea nitrogen concentration [ 23 ]; however, whether this elevation stems from reduced plasma volume, increased protein degradation, or other reasons remains unknown. Thus, blood urea nitrogen (BUN) is used as an indicator of muscle catabolism or breakdown, because tissue degradation results in an increase in BUN [ 21 ]. A review [ 24 ] reviewed that uric acid excretion is increased in stressed poultry owing to corticosterone -driven gluconeogenesis. Other indicators or measures of protein breakdown (muscle catabolism) include increased plasma creatinine, Nt-methyl histidine, creatine, and creatine kinase (CK) concentrations. An increase in these markers has been detected during heat load in chickens, turkeys [ 25 ], cows [ 26 ], pigs [ 27 ], and humans [ 28 ]. The increased level of these parameters indicates enhanced muscle protein catabolism. Insulin stimulates protein synthesis or accretion. However, during heat-load, increased muscle protein degradation causes the liver to utilize available AA as gluconeogenic substrates from the carbon skeleton through the gluconeogenesis pathway [ 19 ]. Under stress conditions, the corticoid hormones (CS, ACTH) suppress the synthesis of tissue proteins and boost proteolysis, as catabolic action is elevated in the blood stream. Glycerol produced from lipid degradation is one of the gluconeogenic substrates and accounts for 20% of the glucose production. Therefore, the other products of protein catabolism are used as substrates for glucose production. First, not only the heart and lung tissue proteins are enhanced by the catabolic transformations of protein composition, but also all tissues except for the nervous system. The muscle tissues (muscle protein) that have the highest body nitrogen content are more sensitive to corticosterone administration, resulting in decreased muscle mass and growth retardation in stressed chickens [ 29 ]. A study [ 30 ] found that feed deprivation reduced protein synthesis in the liver of starved chickens, as well as plasma albumin and total protein levels. A study [ 31 ] indicated that the depletion of plasma free AA, elevated blood uric acid concentration, reduced protein synthesis possibly reflected reduced N retention and more active protein catabolism in broilers challenged by very short-term high temperatures. However, chronic exposure to HS decreased protein digestion, decreased feed digestibility, reduced protein breakdown, reduced protein synthesis in the muscles, and decreased most plasma free AA (especially branched-chain AA and sulfur) [ 32 ], whereas the serum levels of glutamic acid, aspartic acid, and phenylalanine increased [ 33 ]. It was found that protein synthesis and N deposition were depressed and proteolysis increased during HS [ 34 ]. AA catabolism was enhanced under chronic HS [ 13 ]; thus, all plasma free AA concentrations decreased, except for glutamic acid, aspartic acid, and phenylalanine. Based on these studies, protein breakdown may increase rapidly in very short-term HS, resulting in a decrease in protein synthesis and an increase in plasma uric acid levels, but then decrease protein breakdown and maintain uric acid levels around normal concentrations as the thermal stress continues. Two previous studies, one on chickens and the other on turkeys, found that heat stress reduced uric acid levels in the blood, which could be attributed to a lower level of total protein as a result of hypotonic overhydration [ 25 ]. Although no sodium concentration was determined in these studies, water intoxication due to excessive water intake causes overhydration when the amount of water intake exceeds that of water excretion in the kidney. As a result, the sodium level in the blood is diluted, resulting in hyponatremia. As a result, hyponatremia is the most common electrolyte disorder that must be carefully managed [ 35 ]. There is little knowledge about the renal function of broilers in hot climates, especially in terms of compensating for water and electrolyte loss. During acute heat exposure, there were variable changes in urinary electrolyte excretion in chickens. Reduced glomerular filtration rates (GFR), tubular sodium reabsorption rates, and filtered water amounts may help heat-acclimated birds reduce the metabolic heat load associated with active solute recovery from the glomerular ultrafiltrate. When heat-acclimated birds consume excessive water intake to support evaporative cooling, these changes in kidney function are thought to reduce urinary fluid and solute loss [ 36 ]. More research is needed, however, to better explain how various factors may contribute to this evidence. In addition, a study [ 37 ] demonstrated increased uric acid levels in heat stressed chickens. Hence, the application of high-protein diets in HS broilers leads to increased blood plasma uric acid and relieved oxidative stress. Furthermore, the activity of enzymes during AA or protein metabolism under stress conditions has been analyzed. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are intracellular enzymes produced in the liver, skeletal muscles, and heart of poultry, and used as indicators of the liver, muscle, and heart damage [ 38 ]. The rate of protein accretion is always a constant balance between breakdown (protein-lysis) and synthesis (protein-genesis) [ 18 ]. The reduction in protein accretion under conditions of chronic HS is because the rate of protein-genesis is more greatly affected than the rate of proteolysis [ 33 ]. Protein synthesis was reduced more in the breast muscles than that in leg muscles; this may be related to higher oxidative metabolism of the leg muscles and increased glycolytic metabolism of the breast muscle [ 39 ]. Increasing dietary protein content from 20% to 25% at 32 °C did not affect the rate of protein synthesis but did increase muscle protein deposition, possibly by reducing protein breakdown [ 33 ]. The authors of [ 40 ] suggested that energy for protein synthesis at the molecular level may be limited at high temperatures; glucose supplementation improves the growth rate at high ambient temperatures. The effects of HS on protein turnover are controversial but may be related to the magnitude and duration of the heat load producing either a detrimental or therapeutic effect. Both HS and pair feeding reduced the muscle mass of rats; however, pair-fed animals had higher protein degradation, leading to a more severe loss of skeletal muscle that might be attributed to protein preservation triggered by heat exposure [ 41 ]. 5. Heat Shock Proteins Heat stress produces the over-expression of heat shock factors and heat shock proteins (HSP) in bird tissues. HSP regulate multiple molecular pathways in cells in response to stress conditions and change the homeostasis of cells and tissues [ 1 ]. HSP affect mediators of inflammation and infection. HSP are molecular chaperones during increased heat, and offer defense. HSP possess mediated responses to endotoxin stimulated synthesis of cytokine, and [ 42 ] reviewed that HSP 70 overlap with NFκB transcription, leading to the deactivation of the inflammatory response. Intestinal permeability offers new targets for HS remedy. A study [ 43 ] reported that when any living organisms are exposed to HS, the synthesis of most proteins is delayed; however, a group of highly conserved proteins, HSP, is rapidly synthesized. HS causes an increase in HSP synthesis, and are also known as stress proteins [ 44 ]. A study [ 45 ] indicated that HS and subsequent elevated HSP might inhibit muscle mass increase, even with unchanged feed intake. Glutamine seems to have a protective effect on heat-shocked skeletal myotubes by inhibiting protein degradation [ 46 ] and this effect might be mediated by HSPs (primarily HSP70 and HSP25/27), independently of glutamine metabolism based on a nonsufficient-metabolizable glutamine analog to mimic the HSP enhancing effect [ 47 ]. Additionally, a review [ 48 ] reported that increased HSPs defend cells from damage and protect them from apoptosis. HSP 70 is the most common family of HSPs and considered the most conservative, and is plentiful in most living organisms and increases synthesis after cell stress [ 49 ]. Glutamine supplementation has been found to increase HSP expression and improve the stress response [ 47 ]. 6. Physiological Mechanism of Stress Regulation in Poultry According to a review [ 50 ], physiological stress regulation mechanisms are classified into three stages: alarm reaction (neurogenic system), resistance or adaptation (endocrine system), and exhaustion. Under HS in fowls, heat generation and metabolizable energy (ME) intake are decreased, which might be owing to reduced thyroid hormones and corticosterone concentration since those endocrine hormones are related to protein turnover acceleration in muscle and thermogenesis [ 51 ]. During HS in birds, abnormal pathways occur, including gluconeogenesis, and as protein catabolism increases the efficiency of energy absorption is decreased because of the increased energy retention. Therefore, during periods of stress, it is possible for decreases in growth to be accompanied by increases in body fat deposition [ 52 ]. Poultry’s normal body temperature is around 41–42 °C, and the thermoneutral temperature for maximum growth is between 18–21 °C [ 53 ]. The environmental temperature, the thermal neutral zone, and the influence of the ambient temperature on heat production and body temperature are shown in Figure 1 . Poultry produce heat through muscular activity and metabolic processes. The optimum or ideal temperature for performance is 19–22 °C in laying hens, and 18–22 °C in broilers [ 55 ]. Heat produced in the body is lost through conduction, convection, radiation, evaporation, and fecal excretion. Heat loss falls into two main categories. First, sensible heat loss occurs through convection, conduction, and radiation when hens are in a comfortable environment of 21–25 °C, and show optimum growth rate, egg quality and size, quality of egg shell, egg production, and hatchability. Second, insensible heat loss occurs through panting (evaporative heat loss), and begins when the temperature reaches 26.67 °C [ 56 ]. In addition, birds can increase respiration rates up to 10× normal. Additionally, chickens diminish heat by raising and spreading their wings and separating themselves from others. HS has a negative impact on both physiological and behavioral activities. Monitoring these criteria during rearing is critical for identifying HS properties and taking appropriate actions to mitigate the effects of HS while developing high-quality poultry through physiological and management strategies such as heat stress acclimation and poultry housing facilities. 7. Hormonal Responses to Stress and the Hormonal Control of Protein Metabolism Hormone signaling plays a vital role in regulating homeostasis, which includes growth, metabolism, reproduction, and immunity. The overall responses to stress shown in Figure 2 . Rapid endocrine responses are mediated by the sympathetic nervous system activation of the adrenal medulla (SA system). However, the long-term effects are due to the activation of the hypothalamic–pituitary–adrenal cortex axis (HPA axis) and the production of glucocorticoids for long time. The effects of stress on growth performance and reproduction through stress hormonal axis, the reproductive axis, and their interaction are shown in ( Figure 3 and Figure 4 ). The effects of HS on appetite and reproductive hormones are negative. Monitoring appetite and reproductive hormone regulation during rearing are critical for mitigating the negative effects of HS and developing high-quality poultry through hormonal strategies. 8. Assessment of Stress HS has a negative impact on production performance, intestinal health, body temperature, immune responses, appetite hormone regulation, and oxidative properties. It is critical to monitor these criteria during rearing in order to identify HS possessions and take timely action to mitigate the negative effects of high ambient temperature. Stress can be an assessment by three potential methods through behavioral/physiological, endocrine, and metabolic systems measurements. These have been suggested as possible indicators of animal well-being ( Table 1 ) [ 20 ]. In addition, neuropeptide Y (NPY) expression is increased in heat-exposed chick brains. NPY has a hypothermic action through the body temperature and heat stress regulation in chicks [ 58 ]. 9. Nutritional Strategies for Preventing HS in Poultry Nutritional strategies targeted to alleviate and overcome the adverse effects of HS in domestic fowl [ 59 ], include preserving feed consumption, electrolytes, water balance, or even by adding vitamins (as ascorbic acid) and minerals [ 4 , 5 ]. Primary strategies in changing the diet formulation of broilers under constant or cycling high-temperature conditions include the suitable use of protein-rich ingredients (AA and crude protein) [ 12 ]. It is necessary to ensure the balance of certain AA, especially, the arginine: lysine ratio, and the supplementation synthetic methionine to correct any nutritional shortages [ 60 ]. A review [ 61 ] found that when protein is the source of energy, the heat increment or specific dynamic action is much greater than when fat or carbohydrate are the sources of energy. Consequently, there are concerns regarding diet-induced heat production related to protein in hyperthermic broilers. Some authors have mentioned the harmful effects of feeding high protein diets [ 62 ], leading to the recommendation of a reduced protein diet to control further higher thermogenesis [ 63 ]. However, higher dietary crude protein (CP) can compensate reduced AA consumption in stressed broilers, thus it seems to be beneficial in hot conditions, resulting in an improved growth rate [ 64 ]. In addition, a review [ 65 ] reported that limited protein supplementation decreased water drinking under HS and limits broilers’ performance. Therefore, the AA balance plays a chief role in the scientific conflict regarding the proteins needed for hyperthermic poultry, and it is necessary to determine the AA required for thermoneutrality. Additionally, the protein needed can change gradually after HS exposure, depending on the time exposed. Moreover, a study [ 66 ] found lower protein degradation with HS could be normalized with thyroxine supplementation. Dietary supplementation with one or a mixture of functional AA (glutamine, leucine, proline, arginine, cysteine, and tryptophan) is possibly beneficial. First, for ameliorating or reducing health threats during different periods of the life cycle, such as the metabolic syndrome, fetal growth limitation, weaning-associated wasting syndrome and intestinal dysfunction, neonatal morbidity and mortality, diabetes, obesity, infertility and cardiovascular disease. Second, for improving or optimizing the efficiency of metabolic transformations to boost muscle development, meat and egg quality, and milk production, and reducing adiposity by inhibiting excess fat deposition. Thus, AA has important functions in both health and nutrition [ 10 ]. Dietary glutamine supplementation alleviates heat stress, resulting in improved performance and humoral immune response in poultry [ 67 ]. In addition, glutamine minimizes the HS effects in heat-stressed chickens in the first weeks of life [ 68 ]. Besides it plays several roles in the metabolism and homeostasis of tissues. A study [ 69 ] reported that glutamic acid and glutamine supplementation, as a conditionally essential AA in broilers under stress conditions, could be beneficial in improving the growth performance and health. For optimal broiler performance, the use of a high-fat diet (fat is less thermogenic than carbohydrates) with adequate levels of essential AA [ 70 ] has been suggested. However, high lysine or Arg:Lys ratio during HS did not reduce the adverse effects of heat stress or even improve the growth rate. Consequently, there is a further challenge to determine the best nutrient during feeding in many fowls during HS [ 6 ]. The addition of appropriate feed additives may be beneficial in improving intestinal absorption and minimizing the negative effects of HS. The addition of active substances during incubation is the most recent advancement. By instilling thermotolerance in newly hatched birds, these methods are expected to have an impact on the poultry industry. The physiology, production, and immunological response of broilers under heat stress are all affected by the feeding regimen, which should be tailored to the Ross-308 and Cobb-500 strains [ 71 ]. It is necessary to monitor nutritional strategies during nutrition applications in order to prevent HS and produce healthy and comfortable poultry with maintaining feed consumption, dietary adjustments, and appropriate diet formulation. For example, dietary protein-rich ingredients, AA balance, or dietary supplementation with one or a combination of functional AA are all important. Electrolytes, vitamins (such as ascorbic acid), and mineral drinking water supplementation, as well as acid–base balance, are also suggested. 10. Effect of HS on Amino Acids The breakdown of dietary protein results in highly elevated heat generation than that of the catabolism of carbohydrates and fats in poultry under a thermoneutral zone ( Table 2 ). A study [ 73 ] found that feeding broilers more protein than their nutrient requirements did not improve performance at 33 °C. Low protein diets, on the other hand, had a negative impact on broiler performance at high ambient temperatures [ 64 ]. A study [ 74 ] attributed these effects to lower feed consumption, decreased consumption of AA, and therefore poor body weight gain and feed efficiency. According to a review [ 75 ], HS reduced AA levels in the birds including citrulline in chicks’ plasma and leucine in the embryonic brain and liver. As a result, oral L-citrulline increased thermotolerance and decreased body temperature in layer chicks. A review [ 72 ] reported that under HS conditions, broilers aged 21 d–49 d should be fed diets containing 90 to 100 percent of the National Research Council (NRC) [ 76 ] recommended levels of AA and protein in diets containing 13.4 MJ ME/kg. According to previous studies, nutritionists did not compensate for diminished consumption in the hot ambient temperature by elevating protein and AA levels. Therefore, the final impact on growth relies on optimal or ideal protein quantity. The ideal AA composition for the maintenance or production varies with ambient temperature and among species, which can be attributed to metabolic stress alterations ( Table 3 ). The optimal or ideal AA for maintenance varies from the ideal AA for production. Birds require higher methionine and cystine, threonine, and fewer leucines than turkeys and pigs, relative to lysine. Some authors reported that greater lysine or Arg:Lys ratios in broiler diets have a beneficial impact, whereas others showed an adverse effect at HT on gain and breast yield [ 72 ]. Therefore, dietary AA influenced heat generation [ 77 ] and improved broiler performance under high temperatures while decreasing nitrogen excretion by 21% between 28 and 49 days of age [ 78 ]. 11. Future Perspectives and Conclusions In conclusion, this review discusses the impact and consequences of HS in poultry. In addition, previous work was summarized, and some recommendations for developing high-quality and comfortable poultry through physiological (including HSP regulation), hormonal, and nutritional strategies were provided. Although the influence of HS on protein metabolic conversions in poultry can be concluded from this review, the scientific and medical evidence is inconclusive. Thus, further molecular studies are necessary to determine efficient HS regulation strategies, to better clarify the mechanisms involved in HS tolerance, to understand the HSP family as a useful biomarker for detecting HS. Then, for improved production efficacy in poultry, it is necessary to manage heat stress optimally. Recently, researchers interested in exploring a new generation of genetic tools that are capable of clarifying the molecular pathways associated with the heat stress in chickens, are offering new perspectives for the use of these tools in animal breeding. Acknowledgments The authors extend their appreciation to the Deputyship for Research and Innovation, “Ministry of Education” in Saudi Arabia for funding this research work through the project number IFKSURP-322. The authors extend their thanks to the RSSU at King Saud University for their technical support. Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Author Contributions Funding acquisition, M.A.A.-G.; project administration, M.A.A.-G.; writing—original draft, M.M.Q.; writing—review and editing, M.M.Q. and M.A.A.-G. All authors have read and agreed to the published version of the manuscript. Funding This research was funded by Deanship of Scientific Research at King Saud University, grant number IFKSURP-322. Institutional Review Board Statement Not applicable. Data Availability Statement Not applicable. Conflicts of Interest The authors declare no conflict of interest. References 1. Perini F. Cendron F. 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Figure 4 Behavioral and physiological adjustments of chickens at high ambient temperatures and its effects on nutrient intake and utilization. Modified after [ 57 ]. animals-11-01167-t001_Table 1 Table 1 Role of endocrine hormones in protein metabolism and summary of potential methods for assessing stress. Hormones Protein Synthesis Proteolysis Insulin Stimulated Inhibited Glucagon Inhibited Stimulated Epinephrine Inhibited Stimulated Glucocorticoids: ACTH *, CS, and Cortisol Inhibited Stimulated (gluconeogenesis) Thyroid hormones T 4 and T 3 Accelerated skeletal muscle protein turnover and heat production under the hot conditions Growth hormone Stimulated Inhibited

Potential Methods for Assessing Stress

Behavioral/Physiological

Endocrine

Metabolic Systems Activity/sleep patterns Catecholamines Immune function Posture/stereotypes ACTH/CRH, glucocorticoids Disease state Feed and water intake Gonadotrophin/sex steroids Growth performance Heart rate and blood pressure Endorphin (β), renin and prolactin Reproductive performance * abbreviations: ACTH: adrenocorticotropin, CS: corticosterone, CRH: Corticotropin-releasing hormone, T 3 : triiodothyronine, and T 4 : thyroxine, adapted from [ 19 , 20 ]. animals-11-01167-t002_Table 2 Table 2 The biochemical efficiency of absorbed nutrients for ATP and lipid synthesis; reviewed in [ 72 ]. Nutrients Calorific Value (kJ/g) ATP Production (%) Lipid Synthesis (%) Starch 17.7 68 74 Protein 23.8 58 53 Fatty acids 39.8 66 90 animals-11-01167-t003_Table 3 Table 3 Estimated ideal protein ratio for a starting hen, broiler, and pig, expressed as a lysine needed percentage [ 70 ]. Amino Acid Hen Turkeys Broiler Chicken Pigs Lysine 100 100 100 Methionine + Cystine 59 72 60 Threonine 55 67 65 Valine 76 77 68 Arginine 105 105 NA 1 Histidine 36 31 32 Isoleucine 69 67 60 Leucine 124 100 111 Phenylalanine + Tyrosine 105 105 95 Tryptophan 16 16 18 NA 1 = not available.

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# 家禽热应激期间及之后的蛋白质与氨基酸代谢:综述

## 摘要

本综述探讨了环境热应激(现代肉鸡生产者面临的一个突出问题)对蛋白质代谢和肉鸡生产性能的影响,以及激活、控制或减轻应激有害影响的生理机制。此外,本文还分析了在应激条件下聚焦氨基酸(AA)消化率的现有科学文献。此外,AA补充是一种良好策略,可通过将应激维持在最佳水平而非完全消除来增强肉鸡的耐热性、改善状况或控制应激,在家禽育种的成功中发挥着重要作用。家禽维持恒温性,其对热应激的反应主要源于环境温度升高和散热效率低下,这给全球家禽业造成了相当大的经济损失。采食量减少是热应激期间通常观察到的现象,也是肉类生产损失的主要驱动因素。然而,越来越多的证据表明,热应激独立于采食量减少而影响家禽代谢和内分泌特征。总之,高环境温度显著降低了日粮AA摄入量,进而降低了肉鸡的蛋白质沉积和生长。需要进一步研究以确定温暖和炎热气候条件下所需的AA量,并引入与鸡热应激相关的遗传育种工具。

**关键词:** 氨基酸;肉鸡;热应激;耐热性;蛋白质代谢

## 1. 引言

禽肉是膳食蛋白质的重要来源,由于养殖技术的改进、自动化设备、全面均衡的饲养以及其他新技术的发展,该产业已培育出高品质家禽[1]。在过去十年中,热带和亚热带地区的肉鸡生产迅速增长,预计未来将保持强劲的增长势头。然而,根据一项综述[2],高环境温度是家禽和畜牧生产性能面临的最大挑战之一,导致这些国家的生产效率下降。此外,现代商品肉鸡对热应激比前几代更为敏感,这是由于其更高的生产性能、生长速度和饲料转化效率[3]。事实上,商品家禽品系可以达到较高的产量,但其体内代谢相对加速,体温调节能力较差,与本地散养鸡相比对生活环境适应性较差[1]。肉鸡较高的生长速度带来了若干后果,如更高的采食量和代谢率以及内源性产热增加。为减少热负荷并避免热致死亡,可通过减少采食量来实现散热和/或降低产热,但这会导致生长速度下降、终末体重降低、胸肉重量减少,以及母鸡的蛋品质、蛋重和产蛋率下降。此外,采食量减少可能导致营养物质缺乏,如蛋白质、AA和能量[4,5,6]。在环境因素中,热应激对采食量[7]、体重增重和胴体特性[2]产生负面影响。此外,热应激(HS)可能在体内引起氧化应激并产生大量自由基,刺激膜脂质过氧化,从而导致DNA和蛋白质膜的降解[8,9]。在家禽中,暴露于HS时观察到线粒体超氧化物产生作为氧化应激的表现[9]。除了作为蛋白质和肽组分的作用外,某些AA(如谷氨酰胺、半胱氨酸、亮氨酸、精氨酸、色氨酸和脯氨酸)还参与代谢途径的调节,从而影响生长、蛋白质积累、维持、免疫和健康[10]。环境温度影响肉鸡骨骼肌中的蛋白质周转率[11]。不仅蛋白质合成代谢,蛋白质分解代谢也是能量消耗较大的过程。热暴露鸡的生长抑制表现为蛋白质增重和保留降低。高蛋白来源通过改善热应激肉鸡的生长而发挥有益作用[12]。研究表明,HS对肉鸡蛋白质合成的影响大于对蛋白质分解的影响,导致骨骼肌中蛋白质沉积减少。一项综述[11]显示,高环境温度和日粮蛋白质摄入影响肉鸡的肌肉蛋白质周转。在肉鸡中,HS改变肌肉蛋白质和AA代谢,并加速肝脏糖异生以供能[13]。日粮策略,如调整日粮中的能量和蛋白质含量,是缓解家禽热应激和增强肉鸡在此条件下生产性能最实用和首选的方法[14,15]。改善日粮AA的整体平衡比增加总蛋白质摄入更为有效[16]。关于HS对肉鸡蛋白质代谢影响的研究有限。因此,有必要探索使生产者能够有效降低环境HS对肉鸡有害影响的机制或方法,特别是通过肌肉蛋白质积累或降解来影响蛋白质代谢的机制。本综述将聚焦于环境热应激对蛋白质代谢和肉鸡生产性能的影响,以及减轻热应激负面影响的生理机制和营养策略,特别是AA在减轻应激肉鸡HS中的作用。

## 2. 氨基酸和/或蛋白质代谢

AA是大多数生物活动所必需的。AA通过钠依赖性同向转运体、质子动力势、反向转运体和其他AA的梯度被转运至肠细胞顶膜并排出侧基底膜。吸收的AA的代谢命运主要取决于营养物质的可用性[17]。通过分解代谢途径移动的AA最终作为糖异生的前体[13],并贡献了禁食动物总AA损失的40%。蛋白质由游离AA合成,这些游离AA可来自日粮(消化的终产物)或体内AA生物合成的代谢来源。这些AA或通过血液循环或在组织中积累,形成池。这些池中AA的浓度基于得失之间的平衡[18]。日粮AA用于构建肌肉生长所需的蛋白质、膜糖蛋白和参与众多生化过程的酶,并作为DNA/RNA合成的前体[10]。AA在肝脏中分解代谢以整合到蛋白质中,为外周组织供能[13]。蛋白质周转是指蛋白质合成与分解之间的平衡。AA的代谢利用同样具有多样性。合成代谢或蛋白质合成促进日粮AA融合到蛋白质中,或在体组织中生物合成。分解代谢通过蛋白质分解产生氨基基团,进而产生尿素或进一步合成蛋白质。此外,还产生碳骨架分子用于葡萄糖生成(糖生成)或脂肪酸生成(脂生成)、二氧化碳并释放能量。内分泌激素在蛋白质代谢中的作用如表1所示。氮排泄可通过测量蛋白质分解或循环过程中的氮损失来确定蛋白质平衡[18]。内源性或日粮蛋白质在吸收前被水解。禽类组织蛋白质频繁更新,释放内源性AA。此外,许多代谢反应将代谢物转化为非必需AA[18]。近年来,AA不仅作为细胞信号分子和蛋白质磷酸化级联反应发挥作用,还作为基因表达的调节因子。此外,AA是激素合成和其他具有重要生物学意义的含氮元素的基本前体。正常水平的AA及其代谢物,如谷胱甘肽、多胺、牛磺酸、一氧化氮、5-羟色胺和甲状腺激素,对其功能是必需的。然而,AA及其代谢物水平升高,如氨、不对称二甲基精氨酸和同型半胱氨酸,被认为对身体具有致病性,导致氧化应激,并引起心血管和神经系统的疾病和障碍。因此,饲料和血液中AA的理想平衡对体内稳态至关重要。AA不仅作为多肽和蛋白质的构建单元,还调节对生长、维持、免疫和繁殖至关重要的基本代谢途径。这些功能性AA包括谷氨酰胺、亮氨酸、脯氨酸、精氨酸、半胱氨酸和色氨酸[10]。

## 3. 氨基酸的生物合成

禽类和所有脊椎动物与植物和许多细菌不同,无法合成某些AA,因此这些被称为必需AA,是组织通过蛋白质合成进行更新所必需的。因此,必需AA必须在日粮中补充。对于蛋白质合成,所有AA同样重要,因为任何AA的缺失都会干扰合成代谢过程。然而,从营养学角度,AA被分为三组[18]。必需AA必须由饲料提供,可分为两组。一组是严格必需的,因为它们不能从AA代谢中间体合成,如产生糖酵解途径中间体的生糖氨基酸或产生乙酰辅酶A或乙酰乙酸中间体的生酮氨基酸。该组的转氨酶缺失,例如蛋氨酸、赖氨酸、色氨酸、苏氨酸和苯丙氨酸。另一组可能从其前体合成不足,例如甘氨酸、亮氨酸、异亮氨酸、缬氨酸、精氨酸、组氨酸和脯氨酸。半必需AA可从必需AA合成。酪氨酸和半胱氨酸分别来源于苯丙氨酸和蛋氨酸。半胱氨酸由丝氨酸(非必需AA)和蛋氨酸(必需AA)合成。非必需AA容易从中间代谢物或类似的非必需AA合成:前一组包括丙氨酸、丝氨酸、天冬氨酸和谷氨酸;后一组包括天冬酰胺和谷氨酰胺[18]。

## 4. HS对蛋白质代谢或周转的影响

热作为应激因素影响吸收后阶段的蛋白质代谢,因为肌肉分解和瘦组织数量的变化可能发生在不同物种中[21]。在肌肉蛋白质中,RNA/DNA合成能力被HS降低[22]。在环境高热期间,由于肌肉分解过程中血浆标志物增加,肌肉组织分解代谢增强。在泌乳奶牛中,HS增加血浆尿素氮浓度[23];然而,这种升高是否源于血浆容量减少、蛋白质降解增加或其他原因仍不清楚。因此,血液尿素氮(BUN)被用作肌肉分解或分解的指标,因为组织降解导致BUN增加[21]。一项综述[24]指出,由于皮质酮驱动的糖异生,应激家禽的尿酸排泄增加。蛋白质分解(肌肉分解)的其他指标或测量方法包括血浆肌酐、Nτ-甲基组氨酸、肌酸和肌酸激酶(CK)浓度增加。在鸡[25]、火鸡、奶牛[26]、猪[27]和人类[28]中,这些标志物在热负荷期间均检测到升高。这些参数水平的升高表明肌肉蛋白质分解代谢增强。胰岛素刺激蛋白质合成或积累。然而,在热负荷期间,肌肉蛋白质降解增加导致肝脏通过糖异生途径利用可用AA作为糖异生底物,从碳骨架获取[19]。在应激条件下,皮质类固醇激素(CS、ACTH)抑制组织蛋白质合成并促进蛋白分解,因为分解代谢作用在血液中升高。脂质降解产生的甘油是糖异生底物之一,占葡萄糖产量的20%。因此,蛋白质分解代谢的其他产物被用作葡萄糖生产的底物。首先,不仅心脏和肺组织蛋白质通过蛋白质组成的分解转化而增强,除神经系统外的所有组织均如此。肌肉组织(肌肉蛋白质)具有最高的身体氮含量,对皮质酮给药更为敏感,导致应激鸡的肌肉质量下降和生长迟缓[29]。一项研究[30]发现,禁食降低了饥饿鸡肝脏中的蛋白质合成,以及血浆白蛋白和总蛋白水平。一项研究[31]表明,血浆游离AA的耗竭、血尿酸浓度升高、蛋白质合成减少可能反映了暴露于极短期高温的肉鸡中氮保留减少和蛋白质分解代谢更为活跃。然而,长期暴露于HS会降低蛋白质消化、降低饲料消化率、减少肌肉中的蛋白质分解和蛋白质合成,并降低大多数血浆游离AA(特别是支链AA和含硫AA)[32],而谷氨酸、天冬氨酸和苯丙氨酸的血清水平则升高[33]。研究发现,在HS期间,蛋白质合成和氮沉积受到抑制,蛋白分解增加[34]。在慢性HS下,AA分解代谢增强[13];因此,除谷氨酸、天冬氨酸和苯丙氨酸外,所有血浆游离AA浓度均下降。基于这些研究,在极短期HS中,蛋白质分解可能迅速增加,导致蛋白质合成减少和血浆尿酸水平升高,但随着热应激的持续,蛋白质分解减少并将尿酸水平维持在正常浓度附近。两项先前的研究,一项针对鸡,另一项针对火鸡,发现热应激降低了血液中的尿酸水平,这可归因于低渗性过度水化导致的总蛋白水平降低[25]。尽管这些研究中未测定钠浓度,但当饮水量超过肾脏排泄水量时,过量饮水导致过度水化。结果,血液中的钠水平被稀释,导致低钠血症。因此,低钠血症是最常见的电解质紊乱,必须谨慎管理[35]。关于炎热气候条件下家禽肾脏功能,特别是在补偿水和电解质损失方面,目前了解甚少。在急性热暴露期间,鸡的尿电解质排泄发生可变变化。肾小球滤过率(GFR)、管状钠重吸收率和滤过水量的降低可能有助于热适应禽类减少与肾小球超滤液中活性溶质回收相关的代谢热负荷。当热适应禽类摄入过量饮水以支持蒸发冷却时,这些肾脏功能变化被认为可以减少尿液和溶质损失[36]。然而,需要更多研究来更好地解释各种因素如何促成这一证据。此外,一项研究[37]证明热应激鸡的尿酸水平升高。因此,在HS肉鸡中施用高蛋白饮食会导致血浆尿酸增加并缓解氧化应激。此外,还分析了在应激条件下AA或蛋白质代谢过程中酶的活性。天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)是在家禽肝脏、骨骼肌和心脏中产生的细胞内酶,用作肝脏、肌肉和心脏损伤的指标[38]。蛋白质积累率始终是分解(蛋白质溶解)和合成(蛋白质生成)之间的恒定平衡[18]。在慢性HS条件下,蛋白质积累的降低是因为蛋白质生成率比蛋白分解率受到更大影响[33]。与腿部肌肉相比,胸部肌肉的蛋白质合成降低更多;这可能与腿部肌肉较高的氧化代谢和胸部肌肉增强的糖酵解代谢有关[39]。在32°C下将日粮蛋白质含量从20%增加到25%不影响蛋白质合成速率,但确实增加了肌肉蛋白质沉积,可能是通过减少蛋白质分解实现的[33]。文献[40]的作者提出,在分子水平上,高温下蛋白质合成所需的能量可能受限;葡萄糖补充改善了高环境温度下的生长速率。HS对蛋白质周转的影响存在争议,但可能与热负荷的大小和持续时间有关,产生有害或治疗效果。HS和配对喂养均降低了大鼠的肌肉质量;然而,配对喂养的动物具有更高的蛋白质降解,导致更严重的骨骼肌损失,这可能归因于热暴露触发的蛋白质保存[41]。

## 5. 热休克蛋白

热应激在禽类组织中产生热休克因子和热休克蛋白(HSP)的过表达。HSP在应激条件下调节细胞中的多种分子途径,并改变细胞和组织的稳态[1]。HSP影响炎症和感染的介质。HSP在高温期间作为分子伴侣,提供防御。HSP具有对内毒素刺激的细胞因子合成的介导反应,文献[42]综述了HSP 70与NFκB转录的重叠,导致炎症反应的失活。肠道通透性为HS治疗提供了新的靶点。一项研究[43]报道,当任何生物体暴露于HS时,大多数蛋白质的合成被延迟;然而,一组高度保守的蛋白质HSP被迅速合成。HS引起HSP合成的增加,也被称为应激蛋白[44]。一项研究[45]表明,HS及随后的HSP升高可能抑制肌肉质量增加,即使采食量未改变。谷氨酰胺似乎通过抑制蛋白质降解对热休克骨骼肌管具有保护作用[46],这种效应可能由HSP(主要是HSP70和HSP25/27)介导,独立于谷氨酰胺代谢,基于非充分代谢的谷氨酰胺类似物模拟HSP增强效应[47]。此外,一项综述[48]报道,增加的HSP保护细胞免受损伤并防止细胞凋亡。HSP 70是最常见的HSP家族,被认为是最保守的,在大多数生物体中含量丰富,在细胞应激后合成增加[49]。已发现谷氨酰胺补充可增加HSP表达并改善应激反应[47]。

## 6. 家禽应激调节的生理机制

根据一项综述[50],生理应激调节机制分为三个阶段:警觉反应(神经源性系统)、抵抗或适应(内分泌系统)和衰竭。在家禽HS期间,产热和代谢能(ME)摄入降低,这可能由于甲状腺激素和皮质酮浓度降低,因为这些内分泌激素与肌肉中蛋白质周转加速和产热有关[51]。在禽类HS期间,出现异常途径,包括糖异生,随着蛋白质分解代谢增加,能量吸收效率因能量保留增加而降低。因此,在应激期间,生长减少可能伴随体脂沉积增加[52]。家禽的正常体温约为41-42°C,最大生长的热中性温度在18-21°C之间[53]。环境温度、热中性区以及环境温度对产热和体温的影响如图1所示。家禽通过肌肉活动和代谢过程产生热量。蛋鸡的最佳或理想温度为19-22°C,肉鸡为18-22°C[55]。体内产生的热量通过传导、对流、辐射、蒸发和粪便排泄散失。散热分为两大类。第一,当母鸡处于21-25°C的舒适环境中时,通过传导、对流和辐射发生显热散失,表现出最佳生长速度、蛋品质和蛋重、蛋壳质量、产蛋率和孵化率。第二,当温度达到26.67°C时,通过喘息(蒸发散热)发生非显热散失[56]。此外,禽类可将呼吸速率提高至正常的10倍。此外,鸡通过抬起和展开翅膀并与其他个体分离来减少热量。HS对生理和行为活动均有负面影响。在饲养过程中监测这些标准对于识别HS特性并采取适当措施减轻HS影响至关重要,同时通过生理和管理策略(如热应激适应和家禽养殖设施)开发高品质家禽。

## 7. 应激的激素反应与蛋白质代谢的激素控制

激素信号在调节稳态中发挥至关重要的作用,包括生长、代谢、繁殖和免疫。应激的总体反应如图2所示。快速的内分泌反应由交感神经系统激活肾上腺髓质(SA系统)介导。然而,长期效应是由于下丘脑-垂体-肾上腺皮质轴(HPA轴)的激活和糖皮质激素的长期产生。应激通过应激激素轴、生殖轴及其相互作用对生长性能和繁殖的影响如图3和图4所示。HS对食欲和生殖激素的影响是负面的。在饲养过程中监测食欲和生殖激素调节对于减轻HS的负面影响和通过激素策略开发高品质家禽至关重要。

## 8. 应激评估

HS对生产性能、肠道健康、体温、免疫反应、食欲激素调节和氧化特性产生负面影响。在饲养过程中监测这些标准对于识别HS特性并及时采取行动减轻高环境温度的负面影响至关重要。应激可通过三种潜在方法进行评估:行为/生理、内分泌和代谢系统测量。这些已被建议作为动物福利的可能指标(表1)[20]。此外,神经肽Y(NPY)表达在热暴露雏鸡大脑中增加。NPY通过体温和雏鸡的热应激调节具有降温作用[58]。

## 9. 预防家禽HS的营养策略

针对减轻和克服家禽HS不良影响的营养策略[59]包括维持采食量、电解质、水分平衡,甚至通过添加维生素(如抗坏血酸)和矿物质[4,5]。在恒定或循环高温条件下改变肉鸡日粮配方的首要策略包括适当使用富含蛋白质的原料(AA和粗蛋白)[12]。必须确保某些AA的平衡,特别是精氨酸:赖氨酸比例,并补充合成蛋氨酸以纠正任何营养缺乏[60]。一项综述[61]发现,当蛋白质作为能量来源时,热增耗或特殊动力作用远大于脂肪或碳水化合物作为能量来源时。因此,存在与高蛋白日粮相关的热产生问题,特别是在高热肉鸡中。一些作者提到了饲喂高蛋白日粮的有害影响[62],建议采用低蛋白日粮以控制进一步的热产生[63]。然而,较高的日粮粗蛋白(CP)可以补偿应激肉鸡中减少的AA摄入,因此在炎热条件下似乎是有益的,从而提高生长速率[64]。此外,一项综述[65]报道,有限的蛋白质补充减少了HS下的饮水量并限制了肉鸡的生产性能。因此,AA平衡在关于高热家禽所需蛋白质的科学争议中起主要作用,必须确定热中性所需的AA。此外,所需的蛋白质在HS暴露后可根据暴露时间逐渐变化。此外,一项研究[66]发现HS下蛋白质降解降低可通过甲状腺素补充恢复正常。补充一种或多种功能性AA(谷氨酰胺、亮氨酸、脯氨酸、精氨酸、半胱氨酸和色氨酸)的混合物可能是有益的。首先,用于改善或减少生命周期不同阶段的健康威胁,如代谢综合征、胎儿生长受限、断奶相关消耗综合征和肠道功能障碍、新生儿发病率和死亡率、糖尿病、肥胖、不育和心血管疾病。其次,用于提高或优化代谢转化效率以促进肌肉发育、肉和蛋品质以及产奶量,并通过抑制过量脂肪沉积来减少肥胖。因此,AA在健康和营养中均具有重要功能[10]。日粮谷氨酰胺补充可缓解热应激,从而提高家禽的生产性能和体液免疫反应[67]。此外,谷氨酰胺在生命最初几周最小化热应激鸡的HS效应[68]。此外,它在组织代谢和稳态中发挥多种作用。一项研究[69]报道,谷氨酸和谷氨酰胺作为应激条件下肉鸡的条件性必需AA进行补充,可有益于改善生长性能和健康。为获得最佳肉鸡生产性能,建议使用高脂日粮(脂肪的热生成低于碳水化合物)并配合足量的必需AA[70]。然而,在HS期间,较高的赖氨酸或Arg:Lys比例并未降低热应激的不利影响,甚至未提高生长速率。因此,在HS期间确定许多家禽饲喂中的最佳营养素面临进一步挑战[6]。添加适当的饲料添加剂可能有益于改善肠道吸收并最小化HS的负面影响。孵化期间添加活性物质是最新的进展。通过在新孵化的禽类中注入耐热性,这些方法预计将对家禽业产生影响。热应激下肉鸡的生理、生产和免疫反应均受到饲喂方案的影响,应根据Ross-308和Cobb-500品系量身定制[71]。在营养应用过程中监测营养策略对于预防HS和通过维持采食量、日粮调整和适当日粮配方生产健康舒适的家禽是必要的。例如,富含蛋白质的日粮原料、AA平衡或补充一种或多种功能性AA的混合物都很重要。还建议补充电解质、维生素(如抗坏血酸)和矿物质饮水,以及酸碱平衡。

## 10. HS对氨基酸的影响

在热中性区,日粮蛋白质在家禽中的分解产生的热量远高于碳水化合物和脂肪的分解代谢(表2)。一项研究[73]发现,给肉鸡饲喂超过其营养需求的蛋白质在33°C下并未改善生产性能。另一方面,低蛋白日粮在高环境温度下对肉鸡生产性能产生负面影响[64]。一项研究[74]将这些效应归因于采食量减少、AA摄入减少,从而导致体重增重和饲料效率低下。根据一项综述[75],HS降低了禽类中的AA水平,包括雏鸡血浆中的瓜氨酸和胚胎大脑和肝脏中的亮氨酸。因此,口服L-瓜氨酸提高了蛋雏鸡的耐热性并降低了体温。一项综述[72]报道,在HS条件下,21-49日龄的肉鸡应饲喂含有国家研究委员会(NRC)[76]推荐水平的90%至100%的AA和蛋白质的日粮,日粮含有13.4 MJ ME/kg。根据先前的研究,营养学家未通过提高蛋白质和AA水平来补偿高温环境下减少的摄入。因此,对生长的最终影响取决于最佳或理想的蛋白质数量。维持或生产的理想AA组成因环境温度和物种而异,这可归因于代谢应激的改变(表3)。维持的理想AA与生产的理想AA不同。与火鸡和猪相比,禽类相对于赖氨酸需要更多的蛋氨酸和胱氨酸、苏氨酸和更少的亮氨酸。一些作者报道,肉鸡日粮中较高的赖氨酸或Arg:Lys比例具有有益影响,而其他研究则显示高温对增重和胸肉产量有不利影响[72]。因此,日粮AA影响热产生[77],并在高温下改善肉鸡生产性能,同时在28至49日龄期间将氮排泄减少21%[78]。

## 11. 未来展望与结论

总之,本综述讨论了HS在家禽中的影响和后果。此外,总结了先前的工作,并为通过生理(包括HSP调节)、激素和营养策略开发高品质舒适家禽提供了一些建议。尽管从本综述中可以得出HS对家禽蛋白质代谢转化的影响,但科学和医学证据尚无定论。因此,需要进一步的分子研究来确定有效的HS调节策略,更好地阐明HS耐受性所涉及的机制,理解HSP家族作为检测HS的有用生物标志物。然后,为了提高家禽的生产效率,必须最优化地管理热应激。最近,研究人员有兴趣探索新一代遗传工具,这些工具能够阐明与鸡热应激相关的分子途径,为这些工具在动物育种中的应用提供新的视角。

## 致谢

作者感谢沙特阿拉伯王国教育部研究与创新副大臣处通过项目编号IFKSURP-322资助本研究。作者感谢国王沙特大学RSSU提供的技术支持。

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**出版者声明:** MDPI对已出版地图和机构隶属关系中的管辖权主张保持中立。

**作者贡献:** 资金获取,M.A.A.-G.;项目管理,M.A.A.-G.;撰写初稿,M.M.Q.;撰写审阅和编辑,M.M.Q.和M.A.A.-G.。所有作者均已阅读并同意手稿的发表版本。

**资金:** 本研究由国王沙特大学科学研究处资助,资助编号IFKSURP-322。

**机构审查委员会声明:** 不适用。

**数据可用性声明:** 不适用。

**利益冲突:** 作者声明无利益冲突。