高精料飼糧條件下反芻動(dòng)物瘤胃適應(yīng)機(jī)制的解析

梁玉生　李發(fā)弟,2　李　飛*

(1.草地農(nóng)業(yè)生態(tài)系統(tǒng)國家重點(diǎn)實(shí)驗(yàn)室，蘭州大學(xué)草地農(nóng)業(yè)科技學(xué)院，蘭州730020；

2.甘肅省肉羊繁育生物技術(shù)工程實(shí)驗(yàn)室，民勤733300)

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高精料飼糧條件下反芻動(dòng)物瘤胃適應(yīng)機(jī)制的解析

梁玉生1李發(fā)弟1,2李飛1*

(1.草地農(nóng)業(yè)生態(tài)系統(tǒng)國家重點(diǎn)實(shí)驗(yàn)室，蘭州大學(xué)草地農(nóng)業(yè)科技學(xué)院，蘭州730020；

2.甘肅省肉羊繁育生物技術(shù)工程實(shí)驗(yàn)室，民勤733300)

摘要：飼喂高能、高淀粉飼糧是集約化生產(chǎn)中提高反芻動(dòng)物生產(chǎn)性能的常用策略，但高精料飼糧易引起一系列的營養(yǎng)代謝疾病，其中以瘤胃酸中毒最為常見。反芻動(dòng)物瘤胃不僅具有消化、吸收營養(yǎng)物質(zhì)的功能，瘤胃上皮亦是重要的免疫屏障，故瘤胃健康對(duì)反芻動(dòng)物至關(guān)重要。本文主要從反芻動(dòng)物采食高精料飼糧時(shí)其瘤胃組織形態(tài)、瘤胃上皮適應(yīng)分子機(jī)制和瘤胃微生物區(qū)系3個(gè)方面的變化進(jìn)行闡述，以期為高精料飼糧條件下瘤胃適應(yīng)機(jī)制的研究提供參考。

關(guān)鍵詞：反芻動(dòng)物；高精料飼糧；瘤胃酸中毒；上皮轉(zhuǎn)運(yùn)；微生物區(qū)系

生產(chǎn)中為提高反芻動(dòng)物的生產(chǎn)性能和經(jīng)濟(jì)效益，生產(chǎn)者常給動(dòng)物飼喂高能、高淀粉飼糧，即高精料飼糧。由于精料如谷物籽實(shí)具有高淀粉、低物理有效中性洗滌纖維(peNDF)的特點(diǎn)，反芻動(dòng)物攝入過多精料將導(dǎo)致瘤胃內(nèi)揮發(fā)性脂肪酸(VFA)累積，進(jìn)而引起瘤胃pH下降，提高瘤胃酸中毒風(fēng)險(xiǎn)[1-3]。此外，高精料飼喂策略還會(huì)引起其他并發(fā)癥，如采食量下降、蹄葉炎、肝膿腫、乳脂率降低等問題[3-4]。因此，有學(xué)者稱亞急性瘤胃酸中毒(SARA)為高精料綜合征[5]。瘤胃在成年反芻動(dòng)物消化、代謝方面具有重要作用，研究發(fā)現(xiàn)，反芻動(dòng)物采食過量高精料飼糧會(huì)造成瘤胃上皮損傷以及瘤胃微生物群落結(jié)構(gòu)、多樣性和豐度發(fā)生變化，最終使得瘤胃吸收功能紊亂[6-7]，但適當(dāng)提高飼糧中精料含量可促進(jìn)幼齡動(dòng)物瘤胃發(fā)育。因此，理解高精料條件下瘤胃上皮結(jié)構(gòu)、功能以及瘤胃微生物區(qū)系的變化規(guī)律，將為診斷、預(yù)防及治療反芻動(dòng)物消化道代謝疾病提供新思路，減少生產(chǎn)中的經(jīng)濟(jì)損失。

1高精料飼糧飼喂方式下瘤胃的適應(yīng)機(jī)制

1.1瘤胃組織形態(tài)的適應(yīng)

由于谷物的瘤胃發(fā)酵產(chǎn)物含有較多丙酸和丁酸，高精料飼糧可刺激瘤胃乳突發(fā)育，增加單位面積乳突的數(shù)量以及乳突的長度和寬度，提高瘤胃上皮對(duì)VFA的吸收量[8-11]。有試驗(yàn)發(fā)現(xiàn)，干草中添加780 g精料可顯著提高德國奶山羊瘤胃乳突的長度、寬度以及瘤胃黏膜單位面積乳突的數(shù)量[11]。瘤胃上皮可分為角質(zhì)層、顆粒層、棘層和基底層，角質(zhì)層對(duì)瘤胃上皮具有保護(hù)作用，但患SARA的動(dòng)物其瘤胃乳突會(huì)出現(xiàn)角化不全[12-13]。研究表明，患SARA奶山羊的瘤胃上皮角質(zhì)層厚度顯著增加，細(xì)胞間緊密連接程度降低，顆粒層厚度顯著降低，但棘層厚度無顯著變化[14]。飼糧中谷物含量達(dá)65%時(shí)，山羊瘤胃上皮除角質(zhì)層加厚、顆粒層變薄及角化不全外，各細(xì)胞層均有細(xì)胞壞死和細(xì)胞緊密程度降低的現(xiàn)象[15]。圍產(chǎn)期奶牛飼糧突然由低能轉(zhuǎn)為高能時(shí)，其瘤胃乳突復(fù)扁平上皮中的基底層、棘層、顆粒層和角質(zhì)層細(xì)胞之間出現(xiàn)嚴(yán)重分層現(xiàn)象，隨著時(shí)間的推移，瘤胃乳突表面變得越來越僵硬，且最外層的角質(zhì)層細(xì)胞連接較為松散[16]。以上研究表明，瘤胃上皮各細(xì)胞層在適應(yīng)高精料飼糧方面存在差異，且飼糧中精料比例過高會(huì)使瘤胃上皮細(xì)胞的通透性增加，降低瘤胃上皮的屏障功能。這可使微生物或其他有毒物質(zhì)進(jìn)入血液循環(huán)，提高免疫應(yīng)激的風(fēng)險(xiǎn)[17]。

幼齡反芻動(dòng)物的瘤胃形態(tài)結(jié)構(gòu)也受飼糧精料水平的影響。研究表明，飼喂高精料飼糧的斷奶羔羊其瘤胃背囊乳突高度和寬度與飼喂牧草的斷奶羔羊無顯著差異，但其乳突表面積卻呈現(xiàn)增加趨勢；此外，不同飼喂方式下瘤胃乳突顏色也存在差異[18]。乳突顏色是檢測瘤胃上皮角質(zhì)化程度的參數(shù)之一，顏色越深表明瘤胃上皮角質(zhì)化程度越高[13]。研究表明，苜蓿組育肥羔羊的瘤胃乳突面積較高精料全混合飼糧組要大且顏色要深[19]?？傊?，適宜濃度的VFA可刺激瘤胃乳突發(fā)育[12]，但瘤胃中VFA累積超過瘤胃上皮吸收承載能力將導(dǎo)致瘤胃上皮損傷[20]。

1.2瘤胃上皮代謝、增殖和分化適應(yīng)變化的分子機(jī)制

1.2.1對(duì)VFA及氫離子(H+)的吸收與代謝

瘤胃pH降低伴隨著瘤胃上皮組織形態(tài)的變化，此時(shí)，瘤胃上皮中與H+轉(zhuǎn)運(yùn)、VFA吸收及代謝相關(guān)基因的表達(dá)量亦會(huì)發(fā)生相應(yīng)的適應(yīng)性變化[12]。瘤胃VFA有游離VFA和非游離VFA 2種形式，其中以游離VFA為主[21]。瘤胃內(nèi)的H+是由VFA解離而來的，瘤胃上皮的吸收作用在移除瘤胃H+途徑中所占的比例為53%[22]。研究表明，飼喂開食料的犢牛其瘤胃上皮的一元羧酸轉(zhuǎn)運(yùn)蛋白-1(MCT-1)表達(dá)量顯著升高，而鈉離子(Na+)/H+交換蛋白-3(NHE-3)表達(dá)量顯著降低[23]。因?yàn)镸CT-1在轉(zhuǎn)運(yùn)一元羧酸時(shí)會(huì)攜帶H+，其表達(dá)量升高可移除瘤胃中部分H+。若維持瘤胃正常吸收功能，除瘤胃中H+濃度不宜過高，還需保證瘤胃上皮細(xì)胞內(nèi)的離子平衡[24]。細(xì)胞中NHE-3有吸Na+排H+的作用，NHE-3的表達(dá)量降低有利于維持瘤胃上皮細(xì)胞內(nèi)pH的穩(wěn)定[25]。飼糧中精料比例由10%提高到35%時(shí)，山羊瘤胃上皮中一元羧酸轉(zhuǎn)運(yùn)蛋白[MCT-1、一元羧酸轉(zhuǎn)運(yùn)蛋白-4(MCT-4)]、H+轉(zhuǎn)運(yùn)載體[Na+/H+交換蛋白-1(NHE-1)、Na+/H+交換蛋白-2(NHE-2)、NHE-3]、VFA轉(zhuǎn)運(yùn)載體[DRA、推定陰離子轉(zhuǎn)運(yùn)蛋白1(PAT1)、陰離子交換蛋白(AE2)]以及Na+/鉀離子(K+) ATP酶(Na+/K+ATPase)的基因表達(dá)量顯著升高[26]。因?yàn)镹a+/K+ATPase具有吸收細(xì)胞外K+排除細(xì)胞內(nèi)Na+的作用，當(dāng)H+轉(zhuǎn)運(yùn)載體基因表達(dá)量升高時(shí)，細(xì)胞內(nèi)Na+濃度升高，促使Na+/K+ATPase的表達(dá)量升高以保持細(xì)胞內(nèi)Na+/K+的平衡。有研究表明，瘤胃上皮中吸收短鏈脂肪酸(SCFA)相關(guān)基因的mRNA表達(dá)量受瘤胃pH和SCFA濃度的共同作用[26]。目前瘤胃上皮H+吸收方面雖已挖掘出大量相關(guān)基因[27]，但有些基因在瘤胃上皮中的表達(dá)位置并不確定，各基因表達(dá)產(chǎn)物是否存在轉(zhuǎn)運(yùn)特異性或轉(zhuǎn)運(yùn)速率差異還有待進(jìn)一步研究[12]。

反芻動(dòng)物所需代謝能約80%來自VFA，故VFA在反芻動(dòng)物能量供給方面起著重要作用[28]。丁酸可被瘤胃上皮吸收并在瘤胃上皮合成β-羥丁酸(BHBA)，剩余部分會(huì)進(jìn)入到肝臟生成酮體[29]。3-羥基-3-甲基戊二酰乙酰輔酶A合成酶2(HMGCS2)位于線粒體中，是瘤胃上皮生酮途徑中的限速酶[12,30]。但研究發(fā)現(xiàn)，飼喂高精料飼糧的泌乳奶牛和羔羊，其瘤胃上皮HMGCS2的表達(dá)量并未發(fā)生顯著變化[31-32]。以上研究結(jié)果表明，在高精料飼糧條件下瘤胃上皮中HMGCS2 mRNA的表達(dá)量與瘤胃上皮的生酮作用無關(guān)，這可能是用于合成BHBA的底物濃度增加而造成的[32]。

目前瘤胃VFA的吸收相關(guān)研究大都集中在游離VFA上，而反芻動(dòng)物采食高精料飼糧后瘤胃pH會(huì)降低，此時(shí)非游離VFA濃度將升高。非游離VFA主要通過自由擴(kuò)散被瘤胃上皮吸收，該途徑與瘤胃上皮細(xì)胞膜內(nèi)脂類包括膽固醇與磷脂含量有關(guān)。已有學(xué)者對(duì)瘤胃上皮中膽固醇合成相關(guān)基因進(jìn)行了研究[31,33]，但有關(guān)瘤胃上皮磷脂的合成機(jī)制還未見報(bào)道，有待揭示。

1.2.2尿素氮的利用

肝臟合成的尿素可經(jīng)瘤胃上皮和腮腺分泌到瘤胃，是瘤胃微生物生長所需氮素的重要組成部分。尿素轉(zhuǎn)運(yùn)蛋白(UT)可以協(xié)助尿素通過瘤胃上皮[34]。體內(nèi)和體外試驗(yàn)均已證明低pH和高VFA濃度會(huì)提高瘤胃上皮中尿素轉(zhuǎn)運(yùn)蛋白-B(UT-B)的mRNA表達(dá)量和蛋白質(zhì)豐度，并伴隨著G蛋白偶聯(lián)受體(GPR)41和GPR4的mRNA表達(dá)量和蛋白質(zhì)豐度的升高[35]。上述研究表明，不同飼糧構(gòu)成條件下瘤胃上皮中UT-B基因的表達(dá)量受GPR41和GPR4的調(diào)控[35]。此外，研究表明，GPR41和GPR43可能會(huì)影響VFA對(duì)瘤胃發(fā)育、胰島素和胰高血糖素分泌的調(diào)節(jié)作用[36]。因此，VFA、pH、GPR和UT-B之間可能存在著關(guān)聯(lián)性。但UT-B并非轉(zhuǎn)運(yùn)尿素的唯一載體，因?yàn)楫?dāng)其受到抑制時(shí)尿素轉(zhuǎn)運(yùn)并沒有完全停止[37]。水通道蛋白(AQP)可允許尿素的通過，但位于瘤胃上皮的AQP是否具有轉(zhuǎn)運(yùn)尿素的功能并不明確[37]。研究發(fā)現(xiàn)，當(dāng)飼糧突然轉(zhuǎn)變?yōu)橐子诎l(fā)酵的碳水化合物時(shí)，瘤胃上皮的AQP-3和UT-B基因的表達(dá)量呈直線上升趨勢，且基因表達(dá)量要顯著高于高飼草組[37]。因此，除UT-B外，AQP-3在尿素轉(zhuǎn)運(yùn)中也可能發(fā)揮作用。此外，有研究報(bào)道，丁酸可調(diào)節(jié)綿羊體內(nèi)的尿素合成與尿素氮的再分配[38]。但丁酸對(duì)尿素氮再分配的調(diào)控機(jī)理仍不明確，該方面的研究將為理解高精料飼糧模式下瘤胃的適應(yīng)機(jī)制以及能氮平衡提供理論依據(jù)。

1.2.3瘤胃上皮細(xì)胞的增殖與分化

瘤胃上皮結(jié)構(gòu)與功能的維持需要各類細(xì)胞不斷的增殖與分化，該過程受表皮生長相關(guān)基因的調(diào)控[8]，如胰島素樣生長因子結(jié)合蛋白-5(IGFBP-5)、胰島素樣生長因子結(jié)合蛋白-3(IGFBP-3)、胰島素樣生長因子結(jié)合蛋白-6(IGFBP-6)等基因。一般認(rèn)為，丁酸是調(diào)控瘤胃上皮細(xì)胞增殖與分化的重要調(diào)控因子，飼喂高精料飼糧會(huì)使瘤胃中丁酸濃度升高，丁酸可能會(huì)影響到胰島素樣生長因子軸，促使其分泌促細(xì)胞分化的激素，減少促細(xì)胞凋亡激素的分泌[39]。研究發(fā)現(xiàn)，泌乳奶牛在適應(yīng)高精料飼糧過程中瘤胃上皮中IGFBP-5基因的表達(dá)量顯著上升，IGFBP-3、IGFBP-6和橋粒芯糖蛋白-1(DSG-1)基因的表達(dá)量顯著下降，這可導(dǎo)致瘤胃復(fù)扁平上皮的厚度和顆粒層細(xì)胞間黏附性降低，從而增加瘤胃上皮的通透性，最終引發(fā)瘤胃上皮損傷[8]。有研究表明，奶牛在分娩后瘤胃上皮中DSG-1、結(jié)締組織生長因子(CTGF)、角膜鎖鏈蛋白(CDSN)、胰島素樣生長因子結(jié)合蛋白-2(IGFBP-2)、上皮調(diào)節(jié)蛋白(EREG)基因的表達(dá)量顯著升高，而IGFBP-3和表皮生長因子受體(EGFR)基因的表達(dá)量則顯著降低[16]。以上研究表明，pH較低時(shí)瘤胃上皮會(huì)通過上調(diào)細(xì)胞增殖與分化相關(guān)基因的表達(dá)來提高瘤胃上皮的緊密程度，進(jìn)而降低瘤胃上皮的損傷程度。

膽固醇是哺乳動(dòng)物細(xì)胞膜的重要組成成分，但膽固醇含量過高會(huì)引起炎癥反應(yīng)、氧化應(yīng)激、細(xì)胞增殖和遷移，并改變細(xì)胞膜的通透性，最終導(dǎo)致組織損傷[33,40]。3-羥基-3-甲基戊二酰乙酰CoA合成酶1(HMGCS1)位于細(xì)胞質(zhì)中，參與膽固醇的合成。研究發(fā)現(xiàn)，患瘤胃酸中毒的奶牛無論是處于泌乳期還是非泌乳期，HMGCS1基因的表達(dá)量均降低[31,33]。另有研究表明，飼喂高精料飼糧條件下，羔羊瘤胃上皮中HMGCS1基因的表達(dá)量顯著降低[32]。這可能是因?yàn)轱曃垢呔巷暭Z時(shí)，用于合成膽固醇的底物如丙酸、丁酸等SCFA濃度增加，HMGCS1基因表達(dá)量降低可維持瘤胃上皮中膽固醇含量的穩(wěn)定性，以免造成高膽固醇含量對(duì)瘤胃上皮的損傷。

1.3瘤胃微生物區(qū)系的變化

因?yàn)榱鑫肝⑸锛瓤衫锰妓衔飳⑵浒l(fā)酵產(chǎn)生VFA供反芻動(dòng)物利用，又可為宿主提供微生物蛋白，故瘤胃微生物對(duì)反芻動(dòng)物極其重要[41]。當(dāng)瘤胃pH低于6.0時(shí)，纖維分解菌生長受到抑制，而較低pH有利于淀粉分解菌的增殖[41-42]。諸多研究表明，奶牛飼喂高精料飼糧時(shí)瘤胃微生物的密度、多樣性以及微生物群落結(jié)構(gòu)均會(huì)受到影響[43-45]。高精料飼喂條件下奶牛瘤胃內(nèi)容物中固相部分和液相部分的微生物構(gòu)成存在差異，前者的瘤胃微生物密度降低且厚壁菌門的微生物占主導(dǎo)地位，同時(shí)瘤胃中產(chǎn)琥珀酸絲狀桿菌(Fibrobactersuccinogenes)的數(shù)量會(huì)隨著精料采食量的升高而降低[43,45]。研究發(fā)現(xiàn)，隨飼糧中谷物含量的增加原蟲內(nèi)毛目微生物數(shù)量呈增長趨勢，當(dāng)飼糧中谷物含量達(dá)60%時(shí)，普雷沃氏菌屬(Prevotellaalbensis)和產(chǎn)琥珀酸絲狀桿菌的數(shù)量下降，但乳酸桿菌(Lactobacillus)的數(shù)量增加[46]。乳酸桿菌的發(fā)酵終產(chǎn)物主要是乳酸，是引起瘤胃酸中毒的重要因素。瘤胃上皮微生物區(qū)系在反芻動(dòng)物飼喂高精料飼糧前后存在顯著差異[47]。當(dāng)飼糧中谷物含量由3%升高到75%或92%時(shí)，肉牛瘤胃上皮中才會(huì)出現(xiàn)密螺旋體屬(Treponemasp.)、反芻桿菌屬(Ruminobactersp.)和毛螺菌屬(Lachnospiraceaesp.)細(xì)菌[48]。瘤胃酸中毒的嚴(yán)重程度以及誘導(dǎo)瘤胃酸中毒的飼糧差異均會(huì)影響瘤胃微生物群落結(jié)構(gòu)。谷物誘導(dǎo)的重度SARA，瘤胃微生物以牛鏈球菌(Streptococcusbovis)和大腸桿菌(Escherichiacoli)為優(yōu)勢菌群；谷物誘導(dǎo)的中度SARA，瘤胃優(yōu)勢菌群為埃氏巨型球菌(Megasphaeraelsdenii)；苜蓿顆粒誘導(dǎo)的SARA，瘤胃微生物以普雷沃氏菌屬為主[49]。由此可知，瘤胃微生物不僅受到瘤胃pH的影響，而且受飼糧組成的影響。用于微生物發(fā)酵的原料來源和濃度受飼糧組成的影響，故不同飼糧條件下瘤胃微生物區(qū)系可能存在差異。當(dāng)瘤胃pH較低時(shí)，反芻獸新月形單胞球菌(Selenomonasruminantium)的繁殖會(huì)受到抑制，牛鏈球菌占總菌的比例一直較低，這表明除牛鏈球菌外很可能還有其他微生物參與瘤胃酸中毒的形成[50]?？傊?，隨著瘤胃pH的降低，適于在酸性條件下生長的微生物如普雷沃氏菌屬、乳酸桿菌會(huì)大量繁殖，而降解纖維素的微生物如產(chǎn)琥珀酸絲狀桿菌、溶纖維丁酸弧菌(Butyrivibriofibrisolvens)的數(shù)量會(huì)降低。這不僅會(huì)降低反芻動(dòng)物對(duì)粗飼料的消化率，而且會(huì)影響動(dòng)物的健康。理清高精料飼糧條件下消化道微生物區(qū)系的演替以及宿主與微生物之間的相互作用，將為解決高精料飼糧引起的營養(yǎng)代謝疾病提供新思路。

2小結(jié)

綜上所述，反芻動(dòng)物的瘤胃具有適應(yīng)高精料飼糧的機(jī)制，該適應(yīng)機(jī)制是瘤胃結(jié)構(gòu)、功能和微生物區(qū)系三者共同作用的結(jié)果。但該機(jī)制具有一定的局限性，它會(huì)受瘤胃pH和飼糧組分的影響，反芻動(dòng)物攝入過多易發(fā)酵碳水化合物仍會(huì)造成瘤胃消化及吸收功能紊亂。進(jìn)一步系統(tǒng)地研究高精料飼糧條件下瘤胃形態(tài)、VFA吸收以及微生物區(qū)系三者間的相互作用，將為優(yōu)化瘤胃功能提供理論依據(jù)。

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(責(zé)任編輯菅景穎)

Analysis of Rumen Adaptive Mechanism under the Condition of Higher Concentrate Diets

LIANG Yusheng1LI Fadi1,2LI Fei1*

(1. Key State Laboratory of Agro-Ecosystems, College of Pastoral Agriculture Science and Technology,Lanzhou University, Lanzhou 730020, China; 2. Biotechnology Engineering Laboratory of Gansu Meat Sheep Breeding, Minqin 733300, China)

Abstract:Feeding a diet containing higher energy and starch level is a common strategy to improve performance in ruminant production. However, higher concentrate diets can cause the nutritional metabolic disease, especially ruminal acidosis. The rumen not only has the functions of digesting and absorbing nutrients, but also is a significant immune barrier. Thus, rumen health plays an important role for ruminants. This paper mainly elucidated the changes of morphology, molecular adaptive mechanism of rumen epithelium and microbiota of the rumen, aiming at providing some references for rumen’s adaptive mechanism under the condition of feeding higher concentrate diets.[Chinese Journal of Animal Nutrition, 2016, 28(1)：20-26]

Key words:ruminant; higher concentrate diets; ruminal acidosis; epithelial transportation; microbiota

*Corresponding author, associate professor, E-mail: lfei@lzu.edu.cn

中圖分類號(hào)：S816

文獻(xiàn)標(biāo)識(shí)碼：A

文章編號(hào)：1006-267X(2016)01-0020-07

作者簡介：梁玉生(1990—)，男，河北故城人，碩士研究生，研究方向?yàn)榉雌c動(dòng)物營養(yǎng)學(xué)。E-mail: liangysh14@lzu.edu.cn*通信作者：李飛，副研究員，碩士生導(dǎo)師，E-mail: lfei@lzu.edu.cn

基金項(xiàng)目：國家自然科學(xué)基金項(xiàng)目(31260564)；蘭州大學(xué)中央高校基本科研業(yè)務(wù)費(fèi)專項(xiàng)資金(lzujbky-2015-43)；長江學(xué)者和創(chuàng)新團(tuán)隊(duì)發(fā)展計(jì)劃(IRT13019)

收稿日期：2015-07-18

doi：10.3969/j.issn.1006-267x.2016.01.004