随着全球人口老龄化加快,接受外科手术的老年患者比例上升。然而,因机体生理储备下降并常伴基础疾病,其术后营养不良发生率较高[1]。数据显示,老年外科患者术后营养不良发生率在40%～60%,胃肠道等重大手术后半年内仍有51.6%患者存在营养不良现象[2]。此外,术后康复期约半数老年患者面临肌少症或极高营养不良风险[3]。高发营养代谢障碍不仅延缓康复,还增加再入院率及心血管不良事件的风险[1,4]。

从营养学角度分析,手术创伤诱导的高分解代谢状态是老年患者术后营养不良的重要原因之一[5]。由于老年机体合成代谢能力下降及营养储备有限,术后高分解代谢常导致骨骼肌蛋白质大量分解,加快肌少症进展[6]。同时,氨基酸供应不足限制胶原蛋白等结构蛋白合成,影响组织恢复并延缓伤口愈合[7]。此外,蛋白质和能量缺失抑制免疫细胞增殖及免疫活性物质合成,使免疫功能下降,增加术后感染及其他并发症风险[8-9]。因此,针对老年患者术后营养不良开展科学有效的膳食营养干预,对促进康复和改善临床预后具有重要意义[5]。

尽管食源性优质蛋白与生物活性肽在理论上具有促进骨骼肌蛋白合成[10]、改善营养吸收及调节肠道微生态等多重潜在作用[11-12],但其向老年术后功能食品的实际转化仍面临多方面限制。主要体现在3个方面:一是高营养密度需求与老年患者吞咽及消化安全性之间的矛盾;二是活性肽潜在苦味特征与老年人群接受度及依从性不足之间的矛盾;三是热加工过程中蛋白结构致密化与维持高消化吸收效率之间的矛盾。这些因素在不同环节共同限制了靶向营养干预从机制研究向临床应用的有效转化。

为应对这些问题,本研究拟从食品营养学与功能食品开发角度出发,结合老年术后营养不良的发生特点,系统梳理食源性优质蛋白及生物活性肽的关键作用机制,并重点总结当前用于改善其适老化特性的加工技术与配方优化策略[4-5],以期为老年术后精准营养干预产品的开发提供理论依据。因此,阐明老年术后蛋白质消化吸收障碍的发生机制,是制定后续精准营养干预策略的首要前提。

1 老年术后蛋白质消化吸收障碍的营养学机制

老年外科患者术后营养代谢障碍的发生并非单一病理因素导致,而是年龄相关生理功能减退与手术创伤应激共同作用的结果。在围手术期尤其是术后阶段,机体对膳食蛋白的摄取、消化、吸收及利用受多环节影响。老年患者因胃肠道结构与功能生理性衰退,其蛋白质消化吸收能力已呈下降趋势[13]。同时,手术应激诱导高分解代谢状态,促进蛋白质分解并引发负氮平衡[14]。围手术期禁食及抗生素应用等医源性因素可致肠道微生态紊乱,进一步降低营养利用效率[15-16]。这些因素叠加共同导致术后蛋白质稳态失衡及骨骼肌加速流失[17]。因此,本研究从胃肠消化功能衰退、应激代谢调控及肠道微生态紊乱3个方面阐述老年术后蛋白质消化吸收障碍的营养学机制。

1.1 老年术后蛋白质稳态失衡的生理病理基础

老年外科患者的蛋白质稳态受消化吸收能力下降与术后应激性高分解状态的共同影响[18]。随着年龄增长,胃肠道结构与功能逐渐退化,使蛋白质的初始消化效率降低[19],老年人群胃酸(空腹胃液pH值常由青年期的1.5～2.5升至4.0以上)及胃蛋白酶分泌减少40%～50% [20],同时胰蛋白酶(胰蛋白酶分泌量降低25%～40%)与小肠刷状缘肽酶活性降低[21],从而限制了氨基酸与小肽等可吸收底物的生成。未被充分消化的蛋白质进入远端肠道后,还可能增加机体的代谢负担[22]。

1.2 手术应激诱导的高分解代谢机制

在外科创伤条件下,机体的下丘脑-垂体-肾上腺(hypothalamic-pituitary-adrenal, HPA)轴被激活,皮质醇水平升高,并伴随肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)、白细胞介素-6(interleukin-6, IL-6)等炎症因子释放[14],使整体代谢状态向分解方向倾斜。在骨骼肌中,炎症与胰岛素抵抗共同作用,抑制胰岛素样生长因子-1(insulin-like growth factor-1, IGF-1)信号传导,削弱雷帕霉素靶蛋白复合物1(mechanistic target of rapamycin complex 1, mTORC1)介导的蛋白质合成[23]。同时,炎症信号激活泛素蛋白酶体系统及自噬降解途径,促进肌蛋白降解[24]。叉头框O型(forkhead box O, FoxO)转录因子的激活进一步上调肌肉环指蛋白1(muscle RING-finger protein-1, MuRF1)、肌肉萎缩F-box蛋白(muscle atrophy F-box, MAFbx)等基因表达,加速肌原纤维蛋白降解[25]。这些过程导致骨骼肌蛋白合成受抑、分解增加,引发术后肌少症。此外,老年术后组织修复消耗巨大,若外源性补充不足,将因氨基酸匮乏延缓伤口愈合。

1.3 肠道微生态失调对氨基酸代谢的干扰

围手术期干预可影响维持营养代谢稳态的肠道微生态。术前禁食和术后抗生素常导致肠道菌群多样性及产短链脂肪酸菌群丰度下降,影响黏膜屏障与营养吸收[26]。受肠道微环境恶化的影响,肠上皮细胞氨基酸转运蛋白[广泛中性氨基酸转运蛋白1(broad neutral amino acid transporter 1, B0AT1)等]的表达与活性可能受抑制[27],进一步降低氨基酸摄取效率[28]。另一方面,胃肠消化减弱使未完全消化蛋白进入远端肠道,易被条件致病菌利用发生腐败代谢,产生氨、对甲酚及吲哚等代谢物[29]。肠道屏障受损时,这些产物进入循环,加重全身炎症负荷,进一步干扰机体氨基酸代谢与营养稳态[30]。

2 食源性优质蛋白与生物活性肽的精准营养干预策略

针对老年外科患者术后的蛋白质合成抵抗与微生态失衡,多源优质蛋白与食源性活性肽互补为核心的精准营养干预展现出显著优势(表1[31-47])。该干预策略并非单一作用机制的叠加,而是围绕营养供给、体内利用及系统调控等环节构成多层次的协同作用体系。

图1系统解析了食源性优质蛋白与生物活性肽发挥特异性调节作用的分子机制,重点呈现3类作用途径之间的内在关联。图1表明,低聚肽可通过肠上皮PepT1转运体实现高效跨膜吸收,亮氨酸等营养信号进一步激活mTORC1介导的肌肉蛋白合成通路,同时通过调节肠道菌群结构抑制潜在促萎缩代谢产物生成,从而共同参与肠-肌轴的整体调控。上述过程相互衔接,形成有助于缓解老年骨骼肌合成抵抗并促进术后蛋白质代谢稳态恢复的功能网络,体现了活性肽在跨器官代谢调节中的作用优势。

该协同体系按基础供给到系统调控的逻辑层级展开。在供给层,多源蛋白互补实现氮源的连续完整覆盖;在吸收层,低聚肽的高效消化改善了老年跨屏障转运效率;在代谢层,支链氨基酸直接激活骨骼肌合成信号;在系统层,肠-肌轴稳态通过调控微生态与炎症,为肌肉合成提供代谢基础。本节将逐层深入阐述老年术后精准营养干预策略的核心机制。

2.1 动物、植物与微生物来源优质蛋白的消化吸收动力学与围手术期应用

老年围手术期患者普遍存在骨骼肌合成抵抗与蛋白利用率低[17],且其蛋白质需求呈现显著的阶段性特征。术后高应激期(0～72 h)机体处于高分解代谢状态,蛋白质适宜摄入量为0.55～1.50 g/(kg·d)[48];进入恢复期(1～2周),代谢逐渐由分解向合成转变,需求显著增至1.2～2.0 g/(kg·d)[49-50];在恢复后期(2周至数月),为维持肌肉质量与功能重建,摄入量需维持在1.6～2.0 g/(kg·d)的高水平[17],并建议长期结合口服营养补充剂以预防肌肉流失风险。

针对这种随术后时间动态变化的阶梯式高营养需求,单一蛋白质难以兼顾快速合成与氨基酸的持续供给。因此,基于可消化必需氨基酸评分(digesti-ble indispensable amino acid score, DIAAS)及消化吸收动力学差异的多源蛋白组合策略逐渐受到关注。不同来源蛋白质的氨基酸释放速率有显著差异。乳清蛋白消化快,外源性苯丙氨酸出现量在(49±20) min即达峰,短期内提升必需氨基酸水平;酪蛋白及其衍生肽排空慢,其峰值延至(96±72) min,循环中氨基酸供给时间更长[31]。植物源蛋白,例如豌豆蛋白水解物在回肠中与酪蛋白具有相似的平均消化速率,但亮氨酸等特定氨基酸的消化率偏低[51]。基于此,多源蛋白复配已成为常用策略之一,例如大豆蛋白与乳源蛋白组合后,餐后代谢反应较单一蛋白更平稳,合成代谢效应更持久[52]。

此外,部分食源性优质蛋白的活性肽成分还参与氧化应激的调节[53-54]。大豆肽、核桃肽等植物低聚肽具有抗氧化活性[55],可通过调节核因子-κB(nuclear factor kappa-B, NF-κB)信号通路、降低活性氧(reactive oxygen species, ROS)水平[42-43],改善炎症与代谢环境,从而间接提高蛋白质代谢的稳定性。在此基础上,随着可持续蛋白资源开发技术的不断推进,微藻蛋白和微生物蛋白逐渐成为老年营养干预领域的重要蛋白质来源[44-46]。微藻蛋白具有较高的蛋白质含量和较为完整的必需氨基酸组成[44-45],经酶解等加工处理后可促进细胞结构破坏,释放具有抗氧化、抗炎及代谢调节作用的活性肽[45],在功能食品开发和慢性代谢健康管理中展现出应用潜力。微生物真菌蛋白具有独特的菌丝结构,其氨基酸组成较为均衡,并表现出良好的消化利用特性[46]。相关研究发现,真菌蛋白能够促进餐后肌肉蛋白合成[47],为维持老年人群肌肉健康和改善肌少症提供潜在营养支持。此外,部分真菌来源食品富含β-葡聚糖等功能性膳食纤维,具有调节肠道微生态和改善肠道屏障功能的潜力[46]。因此,将微藻蛋白、真菌蛋白与动物源及植物源蛋白进行合理复配,可充分发挥不同蛋白来源在氨基酸组成、消化特性及功能活性方面的互补优势,进一步提升老年膳食蛋白质量,并拓展多源蛋白在精准营养和功能食品制造中的应用价值[56]。但需指出,目前微藻蛋白和真菌蛋白在商业化应用层面仍面临生产成本较高、部分人群接受度不足及致敏性等现实局限,制约了其在老年膳食中的大规模推广[45-46]。

2.2 食源性生物活性肽的吸收优势与干预机制

老年患者消化液分泌减少,致使整蛋白酶解受阻,限制了营养吸收。而食源性肽无须复杂酶解,可直接通过小肠上皮刷状缘的寡肽转运蛋白1(peptide transporter 1, PepT1/SLC15A1)实现主动跨膜转运[57]。即便在衰老或术后炎症应激状态下,肠黏膜PepT1仍能维持一定表达与转运功能[25]。该质子偶联转运机制独立且高效,其跨膜吸收速率通常比等氮游离氨基酸快2～3倍,能量效率显著优于等氮游离氨基酸,为改善老年蛋白质摄取障碍提供了生理学依据[25,57]。

在肠道转运层面,高剂量游离氨基酸易因共用同一类跨膜转运体(碱性氨基酸间的竞争等)而产生载体拮抗效应,进而破坏外周血氨基酸供给的稳态比例。而低聚肽经PepT1转运,避免了此类竞争性抑制,保障了氨基酸的均衡摄入[57]。更为重要的是,特定食源性肽对刷状缘及肠上皮细胞内的肽酶具有耐受性[58]。以富含甘氨酸-脯氨酸-羟脯氨酸(Gly-Pro-Hyp, GPH)的海洋胶原三肽与牛乳酪蛋白衍生短肽(缬氨酰-脯氨酰-脯氨酸 VPP、异亮氨酰-脯氨酰-脯氨酸 IPP等)为例,其序列中脯氨酸残基特有的刚性吡咯环结构,对管腔及胞内二肽酶具有高度抗性,能够以完整寡肽形式经PepT1入血参与代谢修复[35,40] [图1(a)]。此外,大豆肽消化吸收模型表明,分子质量低于500 Da且N端富含亮氨酸(L)、异亮氨酸(I)等疏水性残基的低聚肽,不仅跨膜转运效率更高,还能以完整分子形式穿越肠屏障,并靶向调控核因子κB抑制蛋白(inhibitor of NF-κB, IκB)的磷酸化[37]。这种以完整活性形式入血的特征,是活性肽绕过消化障碍、在特定靶器官发挥信号调控功能的基础[35,58]。

2.3 支链氨基酸介导的骨骼肌合成通路激活

老年外科患者骨骼肌高分解与合成抵抗并存,单纯补充蛋白质难以见效。现有研究表明,食源性肽中富含的支链氨基酸(branched-chain amino acid,BCAA),尤其是亮氨酸不仅是基础代谢底物,更是驱动蛋白质合成的关键信号[32]。以临床营养中广泛应用的乳清蛋白水解肽为例,其天然具备较高的亮氨酸含量,经肠道吸收后可在短时间内使外周血亮氨酸浓度升高[33]。细胞内的高浓度亮氨酸被传感器Sestrin2识别、结合,促使其从GATOR2复合物解离,进而驱动mTORC1在溶酶体表面发生位移并显著激活,使肌肉蛋白部分合成速率每小时提高0.05%～0.08%[32,59]。这种由肽类释放引发的亮氨酸浓度升高,以及Sestrin2的快速感知,是缓解老年肌肉合成生理性障碍的关键生化环节。

mTORC1作为调控代谢的中枢性激酶复合物,被激活后立即启动2条核心的磷酸化级联通路。直接磷酸化70 kDa核糖体蛋白S6激酶(70 kDa ribosomal protein S6 kinase, p70S6K),并诱导真核翻译起始因子4E结合蛋白1(eukaryotic translation initiation factor 4E-binding protein 1, 4E-BP1)发生磷酸化[60]。除动物源肽外,特定植物源活性肽亦具潜力。例如,玉米醇溶蛋白肽因其制备工艺可保留高比例的BCAA,其质量分数常达20%以上,可作为有效的植物源mTORC1激动剂,可在短时间内显著促进p70S6K与4E-BP1的磷酸化[41] [图1(b)]。同位素示踪研究也证实,高度水解的大豆肽也可上调骨骼肌的实际合成速率[61]。因此,乳清肽、玉米肽及大豆肽摄入后能显著促进肌纤维蛋白的合成,具有在围手术期抑制肌肉流失与促进修复的潜力[33,61]。

2.4 生物活性肽对肠道微生态的重塑与肠-肌轴代谢稳态调控

围手术期禁食及抗生素应用常致老年人群肠道微生态失衡[62]。肠-肌轴(gut-muscle axis)是指肠道微生态系统与骨骼肌之间,通过营养代谢产物(短链脂肪酸等)、肠源性激素以及免疫炎症信号等途径实现跨器官信息交流与稳态调节的功能网络。肠道微生态紊乱不仅损伤黏膜屏障,更会通过肠-肌轴影响全身蛋白质代谢稳态[63]。为应对这些病理环节,食源性肽除提供氮源外,还可通过调节微生态与内分泌通路发挥生理调节效应[64]。

食源性肽的益生元效应可修复肠道机械与生态屏障。动物源活性肽(胶原蛋白肽和鸡肉蛋白肽等)可作为共生菌群的特异性氮源,显著提高嗜黏蛋白阿克曼菌的相对丰度[65]。伴随菌群重塑,短链脂肪酸生成增加,在为肠上皮供能的同时,激活AMP活化蛋白激酶(AMP-activated protein kinase, AMPK)通路,促进闭锁小带蛋白-1(zonula occludens-1, ZO-1)、Occludin等紧密连接蛋白的表达与组装。这种黏膜修复作用能减少肠源性内毒素(即脂多糖,lipopolysaccharide, LPS)向门静脉系统的易位,减轻拮抗肌肉合成的系统性炎症[66-67] [图1(c)]。

高效吸收的低聚肽能减少结肠端蛋白质供给,阻断萎缩毒素生成。老年退化肠道消化不全的大分子整蛋白易在远端结肠被发酵,生成硫酸对甲酚和硫酸吲哚酚等高毒性代谢物[29],经肠-肌轴加剧骨骼肌流失。而大豆肽可在小肠近端被高效吸收,切断远端腐败菌氮源,实现空间减毒。这种由吸收优势带来的减毒效应,为术后肌肉合成提供了有利的代谢环节[29,68]。

此外,食源性肽能在肠道局部通过抑制酶及促激素分泌,产生跨器官代谢调节。围手术期的高应激状态常诱发老年人群严重的外周组织胰岛素抵抗,这直接抑制了骨骼肌的蛋白质合成信号。一方面,大豆衍生肽能在小肠腔内竞争性抑制α-葡萄糖苷酶活性,降低餐后血糖波动,从肠道局部改善全身葡萄糖耐量与胰岛素敏感性[38]。另一方面,乳源水解肽或海洋蛋白肽作为配体与L细胞表面的钙敏感受体(calcium-sensing receptor, CaSR)及PepT1结合,显著促进胰高血糖素样肽-1(glucagon-like peptide-1, GLP-1)的分泌[34,69]。而GLP-1入血后能有效改善创伤应激引起的外周组织胰岛素抵抗[34]。由多肽诱导的胰岛素敏化效应改善了肌肉代谢的内环境,与BCAA介导的mTORC1通路互补,辅助缓解老年骨骼肌合成抵抗[34,38]。

2.5 基于营养干预机制的功能食品制造途径

基于优质蛋白与活性肽激活mTORC1合成通路、经PepT1高效吸收及调控肠-肌轴的机制,在向老年功能食品应用转化的过程中,需要平衡加工工艺与功能特性之间的潜在矛盾。热处理、酶法交联、美拉德反应及微胶囊化等现代加工技术虽能改善适老化质构与掩蔽不良风味,但也可能影响蛋白质与多肽的构效关系、消化动力学及生物活性[70]。

例如,在适老化质构优化中,提高谷氨酰胺转氨酶(transglutaminase, TG)交联度虽增加结构稳定性与内聚性,但过度交联会使蛋白质结构致密化,限制消化酶扩散并降低消化效率[71],进而影响DIAAS[72]。同样,利用美拉德反应改善风味虽能生成特征香气,但也会消耗游离氨基[72],从而可能削弱活性肽对mTORC1信号通路的刺激作用[73]。

为实现营养干预策略向功能食品制造的有效转化,近年来食品制造工程围绕非热加工、新型递送体系和个性化制造等方向开展了深入探索。针对老年术后肌肉损失、炎症反应及营养摄入不足等问题,食品设计的侧重点正逐步从单纯的营养补充,转向对功能组分种类、配比及释放行为的精细化调控。非热加工技术能够在较温和条件下调节蛋白质结构及分子间相互作用,改善食品体系的流变特性和质构性能[74],为构建高蛋白、易吞咽食品提供技术支持[75-76]。针对活性肽稳定性不足及感官限制,基于生物高分子材料的递送体系可实现功能组分保护和消化过程中的有效释放,提高其在食品体系中的应用价值[77-78]。此外,3D食品打印等新型制造技术能够结合老年人群吞咽能力和营养需求差异,实现食品结构与营养组成的个性化调控[75-76]。这些技术的发展推动了营养机制研究与食品制造过程的结合,为老年术后功能食品的精准设计提供了新的技术路径。后续研究仍需围绕适老化质构调控、风味优化及微生态调节等关键策略,以更好满足老年患者的实际生理状况和康复需求[75-77]。

3 面向老年术后的功能食品加工与配方设计

营养递送体系若要实现临床转化并发挥实际干预效果,需充分考虑老年患者特有的生理屏障。老年外科患者在双重应激状态下常同时面临营养需求显著增加与咀嚼吞咽功能减退的矛盾,单纯提高配方营养素浓度难以满足临床需求。因此,功能食品的设计在保证高密度活性组分供给的同时,还需匹配老年人的口腔加工能力,以降低吞咽功能减退导致的误吸风险。此外,还须兼顾其感官耐受特征,以克服味觉退化及对多肽苦味的排斥反应。本文重点围绕质构调控、风味分子优化及微生态协同配方等加工策略,系统阐述其在适配老年人生理功能受限条件下的作用机制,并进一步探讨其如何实现活性组分在体内的安全释放与高效利用。

3.1 术后功能食品的营养基质配方设计原则

老年术后功能食品的蛋白质配方设计不应局限于单一营养目标,而应根据术后不同恢复阶段的生理需求进行动态调整。如2.1节所述,术后高应激期(0～72 h)内,机体处于显著的高分解代谢状态,蛋白质需求为0.55～1.50 g/(kg·d),但此阶段肌肉蛋白合成抵抗现象较为明显。因此,配方设计应优先选择消化吸收速度较快且能够快速提高餐后血氨基酸水平的优质蛋白来源,如乳清蛋白[5,79],以促进氨基酸供应,减缓肌肉蛋白分解。同时,应合理控制单次蛋白质摄入量,避免增加机体氮代谢负担,并结合ω-3多不饱和脂肪酸EPA/DHA[80]以及适量碳水化合物和脂质,维持适宜的热氮比,通过能量底物的节氮作用降低蛋白质氧化供能比例[5],从而减轻炎症应激对蛋白质代谢的不利影响。进入术后恢复期(1～2周)后,机体代谢状态逐渐由分解代谢向合成代谢转变,蛋白质需求量提高至1.2～2.0 g/(kg·d)。此阶段的配方设计应适当增加蛋白质供给水平,并重点关注关键功能性氨基酸的补充,尤其是亮氨酸的有效摄入。研究表明,每餐补充3 g亮氨酸或摄入富含亮氨酸的乳清蛋白,可有效激活mTOR信号通路,提高老年人群肌肉蛋白合成效率[79,81]。因此,在满足总蛋白需求的基础上,提高亮氨酸含量有助于增强营养干预效果,促进术后肌肉功能恢复。在术后恢复后期(2周至数月)阶段,为满足1.6～2.0 g/(kg·d)的高蛋白需求,维持肌肉质量并促进功能重建,配方设计需综合考虑蛋白质消化吸收特性及氨基酸释放过程。可通过乳清蛋白与消化吸收速度较慢的蛋白源,如酪蛋白,或具有可持续生产优势和均衡氨基酸组成的蛋白源,如微藻蛋白[42],进行合理复配,以延长餐后氨基酸供应时间,提高蛋白质利用效率[81]。同时,可强化维生素D等功能性营养因子,增强骨骼肌对营养刺激的响应能力,进一步促进肌肉功能恢复[5,81]。由优质蛋白源、阶段化能量供给策略以及功能活性组分共同构建的复合营养体系,是实现老年术后功能食品精准营养支持和促进机体功能恢复的重要基础。

3.2 适老化食品的质构改良技术

针对吞咽困难,常规高蛋白膳食易引发咽部残留或误吸[82],且单纯增补蛋白质会导致硬度骤增与砂砾感。因此,依据国际吞咽障碍饮食标准倡议(international dysphagia diet standardisation initiative, IDDSI)开发安全的软食或流质食品是干预基础。现代技术通过微观结构参数调控流变学特性与内聚力,有效化解了高营养负荷与吞咽安全间的矛盾[82]。

在蛋白质凝胶调控方面,TG酶交联等技术可增强蛋白食团的内聚力与弹性,避免食物吞咽时发生碎片化,从而降低误吸风险[83]。但过度交联会使凝胶过于致密、硬度增加,限制消化酶扩散并降低蛋白质消化率。因此需控制酶法处理强度,平衡内聚力与硬度,使产品符合IDDSI第4级(极度糊状)或第5级(细碎及湿软)的安全标准[82,84]。

此外,多糖-蛋白复合水凝胶体系具有剪切稀化特征,食团在舌颚剪切作用下黏度可迅速且可逆下降[82]。其在吞咽黏膜表面的润滑作用能弥补唾液减少带来的干涩感[84]。同时,辅以微粒化技术控制粒径可改善高浓度蛋白固有的粗糙口感,赋予产品顺滑流动性[84]。这些流变学改良手段不仅有利于保证吞咽安全,还可改善餐食的感官品质与进食体验,从而促进老年患者的营养摄入[85]。

3.3 食源性肽的风味优化技术

生物活性肽可改善术后肌肉衰减,但在酶解中暴露的大量疏水氨基酸残基会产生强烈苦涩味,严重降低老年患者的进食依从性[86]。因此,风味优化须从源头酶解调控、分子共价修饰及空间位阻隔离3个方面考虑[87-89]。

在源头阻断方面,单一内切酶易致多肽疏水苦味末端无序积累。引入外切酶进行二次定向水解,可切除暴露的苦味残基。内、外切酶协同切割能在保留核心活性肽段的前提下,有效降低水解物的感官苦味强度[87-89]。针对已形成的呈味肽,温和条件下的美拉德反应可使还原糖羰基与寡肽游离氨基共价缩合。此修饰不仅消耗了决定苦味的游离氨基(降低36%以上),还生成吡嗪、呋喃等烘焙香气物质,通过味觉与嗅觉双重改善提升感官接受度[88-89]。此外,利用天然蛋白微粒或水/油/水(water-in-oil-in-water, W1/O/W2)双重凝胶乳液对苦味肽进行微胶囊化包埋,可构建双重物理屏障。这种空间位阻效应有效减少了苦味肽与舌根部2型苦味受体(type 2 taste receptors, TAS2Rs)的直接接触[87,89]。该微观隔离效应既遮蔽了苦味,又能抵抗口腔酶降解,实现活性多肽在胃肠道的定点缓释与高效吸收[89]。

3.4 肠道微生态干预在多肽营养与靶向肌肉合成中的潜在作用

老年外科患者围手术期因禁食、应激及抗生素应用,常发生肠道微生态失调与肠黏膜机械屏障损伤[90]。基于肠-肌轴理论,菌群失调导致内毒素易位并诱发全身炎症,直接拮抗骨骼肌合成代谢并加速肌肉萎缩[90]。因此,功能食品设计已由单一的外源氮源补充,转向重塑肠道内环境与靶向营养输送并行的新模式,微生态制剂、特定多肽成为研发重点[90]。该策略核心在于屏障修复、吸收强化与代谢调控的协同增效[91]。微生态重塑是强化多肽跨膜吸收的物理前提。益生菌与后生元不仅能修复肠道机械屏障(紧密连接蛋白网络),还能快速改善受损的局部免疫微环境[92]。健康的黏膜状态,是确保小肠刷状缘转运蛋白PepT1高效表达、实现低聚肽主动跨膜吸收的核心基础[93]。

另一方面,微生态制剂可竞争性阻断肠源性肌肉萎缩毒素的生成,解除骨骼肌代谢抑制[91,93]。体外研究表明,低聚果糖和菊粉可提高双歧杆菌的丰度,抑制腐败菌的生长,显著降低对甲酚和吲哚类毒性代谢物浓度,从而保护肌肉合成通路[91]。最新研究表明,色氨酸衍生毒素(硫酸吲哚酚等)入血后可直接激活骨骼肌细胞中的芳香烃受体(aryl hydrocarbon receptor, AhR)-丙酮酸脱氢酶激酶4(pyruvate dehydrogenase kinase 4, PDK4)轴,引发线粒体功能障碍并诱导肌肉萎缩[91,94]。在恢复微生态稳定与阻断毒素的前提下,肠道屏障的改善为富含BCAA的高活性肽类提供了更有利的跨膜转运微环境,从而更有效发挥缓解术后肌肉流失、促进康复的作用[91,95]。

4 结论与展望

图2展示了基于肠-肌轴系统的老年术后靶向营养代谢干预的主要逻辑。针对老年患者因胃肠功能减退及手术应激导致的骨骼肌快速流失,营养干预不应仅停留在单一氮源补充,而应形成覆盖跨膜吸收效率提升、肌肉合成信号激活以及肠道微生态与炎症稳态调控的综合作用路径。图2整体展示了从病理代谢紊乱向生理稳态恢复转变的关键环节,可为后续适老化功能性食品配方设计与临床转化研究提供机制依据。

老年外科患者因生理储备下降与手术创伤的双重应激,营养不良与肌少症风险高。以优质蛋白与生物活性肽为核心干预物质,通过调节mTORC1通路及肠-肌轴可改善代谢。然而,这一干预策略的转化应用仍面临挑战。

4.1 现有功能食品干预的局限性

1)质构与消化矛盾。为满足IDDSI标准采用的酶法交联导致凝胶过密,限制消化酶扩散,降低优质蛋白与多肽的生物利用度。

2)风味与工艺不足。活性肽苦涩味影响依从性。特异性酶解等风味优化策略在复杂基质中的长效稳定性及工业控制精度有待提升。

3)干预精准度受限。微生态配方多停留在宽泛的益生元效应,缺乏抑制腐败菌群,阻断硫酸对甲酚等萎缩毒素肠源性生成的特异手段。

4.2 未来研发方向

未来需围绕结构设计、递送优化及微生态调控展开探索,以提升整体利用效率与生理适配性。

1)构建非致密流变学体系。质构设计应转向非共价作用。多糖-蛋白质复合凝胶在吞咽时可维持结构防误吸,入胃后非共价作用解离以充分暴露蛋白底物,平衡吞咽安全与消化率。

2)构建多层递送与保护体系。重点开发双重乳液(W1/O/W2)及肠溶纳米包埋体系。通过物理隔离阻断苦味肽与味觉受体(TAS2Rs)接触以掩盖苦味;利用pH值差异实现响应性保护,避免胃液中的活性肽被降解,提升定点释放与PepT1转运,最大限度地提高多肽的生物利用度。

3)构建肠-肌协同干预策略。基于肠-肌轴精细调控代谢。通过膳食底物调节菌群削减有害产物,复配后生元改善肠屏障与局部炎症。在此优化环境中,BCAA及衍生低聚肽可高效实现炎症调节、毒素抑制与合成激活的协同放大。

综合运用流变学结构调控、稳态递送与微生态精准干预策略,可显著提升老年术后干预的生理适配性与利用效率,为下一代术后功能食品开发提供坚实依据。

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Advances in Protein-Based Dietary Interventions for Postoperative Recovery in Older Adults and Age-Friendly Functional Foods

Li He1,*, Liu Shumeng1, Yao Shenghong1, Liu Wanlu1, Ying Zhiwei2, Liu Xinqi1

(1.Key Laboratory of Nutrition and Health for the Elderly, Ministry of Education, Beijing Technology and Business University, Beijing 100048, China;2.Jiangsu Protec Biotechnology Co., Ltd., Suzhou 215400, China)

Abstract： With the accelerating changes in the global population structure, older surgical patients are at an increased risk of postoperative malnutrition and sarcopenia. Hypercatabolism triggered by surgery, impaired gastrointestinal digestion and nutrient absorption, and perioperative gut microbiota dysbiosis are key factors contributing to disrupted protein homeostasis and accelerated skeletal muscle loss in older adults. Precision nutritional intervention strategies based on proteins of superior quality derived from food sources and bioactive peptides for promoting postoperative recovery in older patients were systematically summarized. The underlying molecular mechanisms were emphatically analyzed, including the complementary digestive kinetics of proteins originating from diverse sources, efficient transmembrane absorption of oligopeptides via the peptide transporter 1 (PepT1), activation of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway by branched-chain amino acids to stimulate muscle protein synthesis, and maintenance of homeostasis within the communication axis between the gut-muscle axis. Furthermore, considering the pathophysiological characteristics of dysphagia, impaired mastication, and reduced appetite in older adults, processing technologies and formulation strategies of functional foods for postoperative older adults were systematically summarized, including texture modification through rheological regulation for foods tailored to older demographics, as well as flavor optimization technologies such as controlled enzymatic hydrolysis and covalent encapsulation of bioactive oligopeptides. Finally, current challenges in achieving synergistic intestinal barrier repair, maintaining processing stability, and improving targeting precision were discussed. Future perspectives, including customized rheological design for foods suitable for the elderly, delivery systems targeting specific sites with enhanced stability, and extensive clinical validation, were also proposed to provide scientific guidance for the development of precision nutritional intervention products for postoperative recovery in older adults.

Keywords： postoperative older adults; postoperative malnutrition; protein; bioactive peptides; age-friendly foods; sarcopenia; gut-muscle axis

doi：10.12301/spxb202600375

文章编号：2095-6002(2026)04-0037-14

引用格式：李赫,刘纾萌,姚圣泓,等. 老年术后恢复的蛋白质膳食干预及适老功能食品研究进展[J]. 食品科学技术学报,2026,44(4):37-50.

Li He, Liu Shumeng, Yao Shenghong, et al. Advances in protein-based dietary interventions for postoperative recovery in older adults and age-friendly functional foods[J]. Journal of Food Science and Technology, 2026,44(4):37-50.

收稿日期： 2026-05-27

基金项目： “十四五”重点研发计划项目(2021YFD2100402)。

Foundation： National Key R&D Program of China (2021YFD2100402).

第一作者： 李 赫,男,教授,博士,主要从事植物蛋白加工与营养食品开发方面的研究。

*通信作者。E-mail: lihe@btbu.edu.cn。

中图分类号： TS218; R153.3

文献标志码： A

(责任编辑：张逸群)