CN100393243C - 营养组合物 - Google Patents
营养组合物 Download PDFInfo
- Publication number
- CN100393243C CN100393243C CNB2003801091065A CN200380109106A CN100393243C CN 100393243 C CN100393243 C CN 100393243C CN B2003801091065 A CNB2003801091065 A CN B2003801091065A CN 200380109106 A CN200380109106 A CN 200380109106A CN 100393243 C CN100393243 C CN 100393243C
- Authority
- CN
- China
- Prior art keywords
- milk
- composition
- alimentation composition
- protein
- hydrolysate
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Expired - Lifetime
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Abstract
本发明人发现半乳糖胺肝病的发作可由包含下述基本成分的营养组合物所抑制:乳清蛋白水解产物;可以改善脂类代谢的卵磷脂、油和高油酸脂肪;以及具有胰蛋白酶节省效应的帕拉金糖。另外还发现该营养组合物中所包含的乳清蛋白水解产物可以抑制巨噬细胞中内毒素诱导的TNF-α和白介素6(IL-6)的生产。
Description
技术领域
本发明涉及可用于营养管理和肝病患者治疗的营养组合物。本发明也涉及可用于对经历如手术、感染和烫伤等外来刺激的病人进行代谢和营养调控(metabolic and nutritional management)的营养组合物。另外,本发明涉及可用于炎症病人的病理改善的营养组合物。
背景技术
在肝病营养病理学中,与碳水化合物代谢有关的异常葡萄糖耐受是常见的,这通常归因于糖酵解酶的活性和外周胰蛋白酶敏感性的降低。尤其是在肝硬化中更是如此,肝硬化时能量消耗增加,作为能源物质的碳水化合物的可用性降低。对肝炎和肝硬化时蛋白质代谢的观察显示了由负氮平衡所致的血浆氨基酸失衡(支链氨基酸/芳香氨基酸代谢速率降低(Fischer速率)、蛋白质异化作用增强、高氨血症(hyperammonemia)、以及低蛋白血症(hypoproteinemia)。另外,在脂代谢方面,也观察到了多聚饱和脂肪酸和脂溶性维生素的减少。
肝硬化包括代偿性(compensated)和代偿失调性(decompensated)肝硬化,其在病理学上的差异同样在于代谢和营养调控的不同。代偿性肝硬化可以采用与慢性肝炎非常类似的方法来调控。然而代偿失调性肝硬化是一种慢性肝衰(liver failure)状态,由于蛋白质代谢增强,过量的蛋白质摄入会导致高氨血症。口服支链氨基酸(BCAAs)缬氨酸、亮氨酸和异亮氨酸能够抑制外周组织的蛋白质代谢并增强肝内蛋白质合成。另外,BCAAs在肌肉内代谢生成丙氨酸,丙氨酸激活肝内葡萄糖合成作用(葡萄糖-丙氨酸循环),并且提高碳水化合物作为能源物质的效率。因此,BCAA产品(HepanEDR,Aminoleban ENR:50-150g/天)被用来弥补骨骼肌中能量的不足。
另一方面,当活体经历如手术、感染、或者烫伤等过度的外来刺激时,局部和全身的炎症介导物质的产生增强。特别是细胞因子是包括循环、内分泌、免疫和代谢等系统中多种反应的重要介导物质。
通常,经历外来刺激时的代谢反应在特征上包括机体尤其是骨骼肌蛋白质分解增强,由于脂质分解所致的甘油和脂肪酸的产生增加,肝脏中糖再生作用、应急蛋白和清蛋白生产的增强。在外来入侵时细胞免疫和体液免疫被抑制,预期免疫相关蛋白的合成减少而蛋白质代谢相当程度地增强。
在遭受外来刺激的机体中,不同细胞因子在代谢变化中的作用已经在阻断细胞因子的生产或活动等的试验中得到揭示,在这些试验中细胞因子本身被给予机体。特别地,由TNF-α、IL-1、和IL-6引起的代谢变化为:(1)与葡萄糖代谢相关的肝糖分解作用增强、高血糖症和低血糖症,(例如,Meszaros K等″Tumor necrosis factor increases invivo glucose utilization ofmacrophage-rich tissues″Biochem.Biophys.Res.Commun.,Vol.149,No.1:pp.1-6,1987 November 30;Tracey,KJ等″Shock and tissue injury induced byrecombinant human cachectin″Science,Vol.234,No.4775:pp.470-474,1986October 24;Fukushima,R等″Different roles of IL-1 and TNF onhemodynamics and interorgan amino acid metabolism in awake dogs″Am.J.Physiol.,Vol.262,No.3,Pt.1:pp.E275-E281,1992 March),(2)与氨基酸和蛋白质代谢相关的肌肉退化和氨基酸释放增加、谷氨酸盐的肠吸收增加、丙氨酸肠释放增加、肝氨基酸吸收增加、以及急性期蛋白合成增强,(例如,Fukushima,R等″Different roles of IL-1 and TNF on hemodynamics andinterorgan amino acid metabolism in awake dogs″Am.J.Physiol.,Vol.262,No.3,Pt.1:pp.E275-E281,1992 March;Moldawer,LL等″Interleukin 1 andtumor necrosis factor do not regulate protein balance in skeletal muscle″Am.J.Physiol.,Vol.253,No.6,Pt.1:pp.C766-C773,1987 December),和(3)与脂代谢相关的脂肪酸降解增强和脂蛋白脂肪酶活性增强(例如,Feingold,KR等″Multiple cytokines stimulate hepatic lipid synthesis in vivo″Endocrinology,Vol.125,No.1:pp.267-274,1989 July;Grunfeld,C等″Tumor necrosis factor:immunologic,antitumor,metabolic,and cardiovascular activities″Adv.Intern.Med.,Vol.35:pp.45-71,1990;Feingold,KR等′Tumor necrosis factorstimulates hepatic lipid synthesis andsecretion″Endocrinology,Vol.124,No.5:pp.2336-2342,1989 May)。
一种阻止遭受外来刺激时由细胞因子引起的代谢异常和器官损伤合理途径就是局部地使细胞因子生产正常,同时阻止细胞因子向全身扩散。这样的方法包括使用肠营养、ω-3脂肪酸、或生长激素的。
有几篇关于在遭受外来刺激时,由于营养给予方式的不同而导致细胞因子的生产产生差异的报导。通过肠或静脉途径给予营养一周时间,在未遭受外来刺激的成年人体内没有发生任何明显的TNF-α和IL-6血液水平差异(如,Lowry,SF等″Nutrient modification of inflammatory mediatorproduction″New Horiz.,Vol.2,No.2:pp.164-174,1994 May)。然而据报导,当通过肠或静脉途径给予营养7天然后静脉注射内毒素时,肠途径给予营养要比静脉途径给予营养时的全身性反应包括发烧以及TNF-α与紧张性刺激激素释放作用温和(如,Fong,YM等″Total parenteral nutrition and bowelrest modify the metabolic response to endotoxin in humans″Ann.Surgery.,Vol.210,No.4:pp.456-457,1989 October)。
发明内容
本发明的一个目的是提供营养组合物用于肝衰的营养调控和治疗。此外,本发明的另外一个目的是提供用于对遭受强烈外来刺激(highly invasivestresses)如手术、感染和烫伤的病人进行代谢和营养调控的营养组合物。进一步,本发明的另一个目的是用于炎症病人病理学改善的营养组合物。
本发明人发现半乳糖胺(galactosamine)诱导的大鼠肝损伤的发作能够被由包含乳清蛋白水解产物、卵磷脂(lecithin)、富含油酸的油、和帕拉金糖(palatinose)等基本成分组成的营养组合物所抑制。另外,他们还发现乳清蛋白水解产物抑制LPS诱导的TNF-α和白介素6(IL-6)在体内的生产。这些结果显示本发明的营养组合物对肝病患者的营养调控与治疗,对遭受强烈外来刺激如手术、感染或烫伤的病人的代谢和营养调控,以及对炎症疾病的病理改善等方面是有用的。
具体地,本发明包括:
(1)用于肝病患者的营养组合物包含:作为蛋白质成分的奶蛋白水解产物和源于发酵奶的蛋白质;作为脂质成分的富含油酸的油和奶卵磷脂和/或大豆卵磷脂;和作为碳水化合物成分的帕拉金糖;
(2)根据(1)的营养组合物,其中所述的奶蛋白选自由酪蛋白、奶蛋白浓缩物(MPC)、乳清蛋白浓缩物(WPC)、乳清蛋白分离物(WPI),α-乳清蛋白(α-lactoalbumin)、β-乳球蛋白(β-lactoglobulin)、和乳铁蛋白(lactoferrin)所组成的组中的蛋白;
(3)根据(1)的营养组合物,其中所述的源于发酵奶的蛋白质源于一种发酵奶中乳清减少的组合物;
(4)根据(1)的营养组合物,其中所述的源于发酵奶的蛋白质源于新鲜干酪;
(5)根据(4)的营养组合物,其中所述的新鲜干酪是夸克(quark);
(6)根据(1)的营养组合物,其中所述的奶蛋白水解产物可以通过用源于地衣芽孢杆菌(Bacillus licheniformus)的alkalase和源于猪胰腺的胰蛋白酶(trypsin)来水解乳清蛋白分离物(WPI)而获得;
(7)根据(6)的营养组合物是使用分级分子量为10,000的超滤膜进一步处理而获得的滤过液;
(8)根据(7)的营养组合物,其中反相HPLC分离层析谱如图1所示;
(9)用于处于高度外来刺激水平的病人的营养组合物,其中所述的营养组合物包含:作为蛋白质成分的奶蛋白水解产物和源于发酵奶的蛋白质;作为脂质成分的富含油酸的油和奶卵磷脂和/或大豆卵磷脂;和作为碳水化合物成分的帕拉金糖;
(10)根据(9)的营养组合物,其中所述的奶蛋白选自由酪蛋白、奶蛋白浓缩物(MPC)、乳清蛋白浓缩物(WPC)、乳清蛋白分离物(WPI),α-乳清蛋白、β-乳球蛋白、和乳铁蛋白所组成的组中的蛋白;
(11)根据(9)的营养组合物,其中所述的源于发酵奶的蛋白质源于一种乳清减少的组合物;
(12)根据(9)的营养组合物,其中所述的源于发酵奶的蛋白质源于新鲜干酪;
(13)根据(12)的营养组合物,其中所述的新鲜干酪是夸克;
(14)根据(9)的营养组合物,其中所述的奶蛋白水解产物可以通过用源于地衣芽孢杆菌的alkalase和源于猪胰腺的胰蛋白酶来水解乳清蛋白分离物(WPI)而获得;
(15)根据(14)的营养组合物是使用分级分子量为10,000的超滤膜进一步处理而获得的滤过液;
和(16)根据(15)的营养组合物,其中反相HPLC分离层析谱如图1所示。
1.蛋白质
1-1.奶蛋白水解产物(Milk protein hydrolysate)
酪蛋白,乳清蛋白(乳清蛋白浓缩物(WPC),乳清蛋白分离物(WPI),α-乳清蛋白(α-La)、β-乳球蛋白(β-Lg)、奶蛋白浓缩物(MPC或总奶蛋白(TMP)),等这些蛋白可以作为蛋白质来源。
正常情况下用于水解乳清蛋白的酶为例如胃蛋白酶、胰蛋白酶、和糜蛋白酶。然而也有将植物来源的木瓜蛋白酶以及细菌和真菌来源的蛋白酶用于研究的报道(Food Technol.,48:68-71,1994;Trends Food Sci.Technol.,7:120-125,1996;Food Proteins and Their Applications:pp.443-472,1997)。乳清蛋白水解酶活性差异很大。胃蛋白酶降解已变性的α-La和α-La,但不能降解天然的β-Lg(Neth.Milk dairy J.,47:15-22,1993)。胰蛋白酶缓慢水解α-La但很难降解β-Lg(Neth.Milk dairy J.,45:225-240,1991)。糜蛋白酶快速降解α-La,然而降解β-Lg缓慢。木瓜蛋白酶水解牛血清白蛋白(BSA)和β-Lg,但α-La对其显示抗性(Int.Dairy Journal 6:13-31,1996a)。然而,在酸性pH条件下,未结合Ca的α-La被木瓜蛋白酶完全降解(J.Dairy Sci.,76:311-320,1993)。
通过控制奶蛋白的酶学降解和修饰奶蛋白,可以在较宽pH范围和处理条件下改变该蛋白的功能性特征(Enzyme and Chemical Modification ofproteins in Food proteins and their Applications pp.393-423,1997 MarcelDekker,Inc.,New York,1997;Food Technol.,48:68-71,1994)。
肽链的水解增加带电基团的数目和疏水性,减小分子量,并且改变分子结构(J.Dairy Sci.,76:311-320,1993)。功能性特征的变化很大程度上依赖于水解程度。通常所观察到的乳清蛋白功能的最大变化是溶解性增加和粘性减小。通常,在水解程度较高时,水解产物不发生沉淀,即使在加热情况下也是如此,在3.5-4.0的pH值条件下高度可溶。水解产物具有比完整蛋白质低得多的粘性。当蛋白质浓度高时这种差异尤其明显。其他的效应包括胶凝特性改变、热稳定性增加、乳化和泡沫化能力增强、乳液和泡沫稳定性降低(Int.Dairy journal,6:13-31,1996a;Dairy Chemistry 4,pp.347-376,1989;J.Dairy Sci.,79:782-790,1996)。
已经知道多种源于奶蛋白的生物活性寡肽((Yoshikawa,M,″NewHorizon in Milk Science″,Yoshikawa,M.ed.,pp.188-195,Kougaku Shuppan,1998;Otani,H.,″New Horizon in Milk Science″,Yoshikawa,M.ed.,pp.97-99,Kougaku Shuppan,1998;Otani,H.,Milk Science,47:183,1998;Trends inFood Science and Technology,9:307-319,1998)。一个这样的例子是具有血管紧缩素转换酶(ACE)抑制剂活性(高血压效应)的肽。
有一些关于多种可能具有ACE抑制剂活性的肽的报道,这些报道是通过体外检测来推测的(例如,J.Dairy Res.,67:53-64,2000;Br.J.Nutr.,84:S33-S37,2000)。也有一些采用不同层析技术纯化和鉴定源于水解产物的ACE抑制性肽的研究报告(for example,Maruyama,S.,&Suzuki,H.,Agricultural and Biological Chemistry,46:1393-1394,1982;Miyoshi S.etal.,Agri.Biol.Chem.,55:1313-1318,1991;Food Science and Biotechnology,8:172-178,1999;Biosci.Biotech.Biochem.,57:922-925,1993)。
根据这些报道,认为ACE抑制剂活性存在于基于柱分离的许多分级成分中。因此,ACE抑制性物质的分子特征是多种多样的。事实上,发现ACE抑制可见于多种蛋白质、蛋白酶以及在水解条件下产生的水解产物。这个事实提示,具有不同氨基酸序列的多种肽都可以具有ACE抑制活性。由于这些肽的化学多样性,层析法纯化水解产物经常伴随着一部分活性肽的损失。在水解过程中,ACE抑制活性不断地产生和降解。当这两种进程达到最优化时,获得最大的水解产物活性。ACE抑制活性通过测定所有的水解产物肽组合物来获得,它依赖于水解酶的特异性和处理条件。
有一篇报道涉及乳清蛋白水解产物最佳化(采用表面响应方法学,response surface methodology)以使ACE抑制活性最大化并且使所需的水解保持在最小程度(International Dairy Journal 12:813-820,2002)。
本发明首次揭示了奶蛋白水解产物抑制LPS诱导的TNF-α和IL-6的体内生产。有一些关于来源于奶蛋白的肽对细胞因子生产的影响的报道。有文献报道,源于牛酪蛋白的肽增强LPS诱导的TNF-α和IL-6在鼠骨髓巨噬细胞中的生产(J.Sci.Food Agric.,81:300-304,2000)。还有文献报道,响应LPS刺激而诱导IL-6生产的肽存在于由益生菌乳杆菌发酵的奶的上清(Milchwissenschaft,57(2):66-70,2002)。然而,就发明人所知,目前尚无有关奶衍生蛋白抑制炎症细胞因子生产的报道。除了具有上述的ACE抑制活性的肽外,抑制LPS诱导的TNF-α和IL-6生产的肽也可能存在于不同柱分离方法中所获得的许多分级成分中。
因此,以对LPS诱导的TNF-α和/或IL-6生产的抑制效应为指针,可以参考上述的文献来优化奶蛋白水解的条件(变性温度、pH、温度、水解时间和酶/底物比)(International Dairy Journal 12:813-820,2002)。因此,本发明包括由此获得的优化的水解条件。
除了上述引用的文献,还存在许多有关奶蛋白水解产物的专利(出版的专利申请和专利)。例子包括:涉及酪蛋白和乳清蛋白的分别水解、继而吸附去除疏水成分、然后将酪蛋白和乳清蛋白以指定比例混合的专利(JP2,986,764);用芽孢杆菌和放线菌蛋白酶水解乳清蛋白、继而去除酶和不溶性水解产物的专利(JP 3,222,638);有关肽混合物的专利,其中由β-Lg降解产生的支链氨基酸/芳香氨基酸的摩尔比为10%或更高,其中芳香氨基酸少于2.0%,混合物的平均分子量为几百到几千(JP 3,183,945);有关乳清蛋白中β-Lg的选择性酶学降解的专利(JP 2,794,305);使用来自地衣芽孢杆菌(B.licheniformis)和/或枯草芽孢杆菌(B.subtilis)的蛋白酶,采用non-pH-stat技术水解乳清蛋白至15%~30%(葡萄糖当量;DE),然后获得截留分子量值大于10,000的超滤膜滤过液(JP 3,167,723);本发明包括除这些专利和专利申请之外的专利和未审公开专利。
上述文献、专利和专利申请中所述的水解产物是否抑制LPS诱导的TNF-α和IL-6的生产可以使用已知的检测系统来测定(如,ExperimentalMedicine Supplementary Vol.″Bio Manual UP Experiment Series″,CytokineExperiment Methods,Miyajima,A.,Yamamoto,M.ed.,Yodosha,(1997))。因此,本发明包括具有抑制TNF-α和IL-6生产的活性的水解产物。
选择例如预热、酶底物比(E/S)、pH、水解温度和水解时间作为条件优化的五个参数。
预热:65-90℃
E/S:0.01-0.2
pH:2-10
水解温度:30-65℃
水解时间:3小时至不足20小时
所使用的酶包括下述来自Nova Nordisk的酶:
1)内切蛋白酶
地衣芽孢杆菌来源的:Alcalase
迟缓芽孢杆菌来源的:Esperase
枯草芽孢杆菌来源的:Neutrase
细菌来源的:Protamex
猪胰腺来源:PTN(胰蛋白酶)
2)外切蛋白酶
米曲霉来源的:Flavorzyme
猪或牛内脏来源:羧肽酶
除上述之外的酶的例子包括动物来源的胰酶制剂(pancreastin)、胃蛋白酶、植物来源的木瓜蛋白酶、菠萝蛋白酶、微生物(如,乳杆菌、酵母、霉菌、分支杆菌)来源的内切蛋白酶和外切蛋白酶、以及它们的粗制纯化物和细菌匀浆物。另外,在联合用酶时也经常使用地衣芽孢杆菌来源的Alcalase和猪胰腺来源的PTN(胰蛋白酶)的酶混合物。
本发明的蛋白质水解产物包括:本身抑制LPS诱导的TNF-α和/或IL-6生产的酶水解产物;超滤所得的残余溶液或滤液;以及显示类似活性的商业奶蛋白水解产物。
奶蛋白水解产物的含量估计为每100mL产品0.9至3g,或者优选1.2至2g。最适范围可用实验确定(如,用对TNF-α生产的抑制作为指标)。
1-2.发酵奶来源的蛋白质(Fermented milk-derived proteins)
发酵奶(酸牛奶(yogurt))来源的蛋白质的氨基酸值为100,其被消化吸收的能力通过发酵得到提高,具备较高营养价值。成分包括去除发酵奶中含水部分(乳清)后的成分(如,JP 3,179,555)。
尽管有许多种的新鲜干酪,包括农家干酪(cottage)、夸克、string、纽沙特尔干酪(neuchatel)、奶油干酪(cream cheese)、mozzarella、意大利乳清干酪(ricotta)、以及意大利牛奶软干酪(mascarpone),而夸克是最适宜的来源。生产夸克的方法是熟知的(如,特开平6-228013)。
每100mL产品中源于发酵奶的蛋白质的含量可以为2-6g或优选2.5-4.5g蛋白质。
2.脂类
2-1.磷脂
奶来源的卵磷脂与大豆或蛋黄来源的卵磷脂联合用作磷脂。也可单独使用奶来源的卵磷脂。在如生化、药学和药理学领域,术语“卵磷脂(lecithin)”仅用于指“磷脂酰胆碱”。然而在商业或工业领域,卵磷脂(lecithin)是作为磷脂酰胆碱、磷脂酰乙醇胺、磷脂酰肌醇、磷脂酸、以及其他磷脂(phospholipid)的混合物的通称来使用的。在“Japan’s Specifications andStandards for Food Additives”,7th edition(1999)中,卵磷脂是指“从油籽或动物来源获得的物质,主要成分是磷脂”。本发明中,奶来源的磷脂也统称“奶来源的卵磷脂”。
奶来源的卵磷脂
奶磷脂(奶卵磷脂)包括鞘磷脂(SM)、磷脂酰胆碱(phosphatidylcholine,PC)、磷脂酰乙醇胺(phosphatidylethanolamine,PE)、磷脂酰肌醇(phosphatidylinositol,PI)、磷脂酰丝氨酸(phosphatidylserine,PS)和溶血磷脂酰胆碱(lysophosphatidylcholine,LPC),它们只存在于乳脂球膜(milk fatglobule membranes,MFGM)。MFGM磷脂分级成分的组成列于表1(Bulletinof Japan Dairy Technical Association,Vol.50:pp.58-91,2000)。
如表1所示,奶磷脂特征性地包含大量SM,大豆卵磷脂中不含SM。对大鼠给予奶卵磷脂时脑和肝中DHA含量的增加程度远大于对大鼠给予大豆卵磷脂时的增加程度。而且,与大豆卵磷脂或蛋黄卵磷脂相比,奶卵磷脂在改善高血脂和脂肪肝方面更为有效。另外,已知SM与胆固醇代谢有关,例如,SM调节胆固醇合成中的HMG-CoA还原酶的活性,也与肠道胆固醇的吸收调节有关。从而认为SM可以进一步增强PC和PE改善脂质代谢的能力(Sasaki,H.,Milk Science 51(2):93-94,2002)。
表1
磷脂成分 | 重量% |
鞘磷脂磷脂酰胆碱磷脂酰乙醇胺磷脂酰肌醇磷脂酰丝氨酸溶血磷脂酰胆碱 | 2236271142 |
富含MFGM的物质的例子包括,联合进行超滤(UF)和微过滤(MF)产生的冻干WPI副产品(MF残留液)、从奶油或黄油中去除脱水乳脂肪(AMF)后得到的分级成分(黄油乳清,butter serum)、从奶油乳清中去除AMF得到的分级成分(奶油乳清,whey cream serum)。以这些物质为原料制备磷脂浓缩物的方法是已知的(如,JP-AHei7-173182包含于本发明)。
大豆卵磷脂
大豆卵磷脂被广泛用作食物和食品领域的天然食物添加剂,而多烯卵磷脂酰胆碱也被用作药物(用途:用于改善肝功能、脂肪肝和慢性肝病的高血脂)。大豆卵磷脂的生理功能的例子包括调节生物膜的形态和功能,改善肺功能、动脉硬化、脂代谢、肝脂代谢,改善和促进神经功能(Food Processingand Ingredients,Vol.29(3):18-21,1994)。
“天然”卵磷脂产品正常情况下按照他们的PC含量归类。根据其用途产生了不同类型卵磷脂的等级。如表2所示,以大豆卵磷脂纯化和分级分离为基础,根据大豆卵磷脂产品中主要成分PC的差异很方便地对其进行了分类(Fujikawa,T.,Oil Chemistry,Vol.40(10):951-958,1991)。
表2
类型 | PC含量(%) |
粘性卵磷脂纯化的卵磷脂提取的卵磷脂PC浓缩卵磷脂PC高度纯化卵磷脂磷脂(PC、PE、PS、PG等) | 15-2020-2530-4045-6075-95分别(individually)为98%或更高 |
奶卵磷脂和大豆卵磷脂可以单独使用或联合使用。每100mL产品的总含量可以为0.1-0.5g,或优选0.2-0.3g。油酸含量可以为2-3g,或优选2.1-2.5g。
2-2.其他脂类
健康、劳动与福利部推荐的饱和脂肪酸(SFA:棕榈酸,硬脂酸等):单价不饱和脂肪酸(MUFA:油酸等):多价不饱和脂肪酸(PUFA:亚油酸、亚麻酸等)优选摄入比率从先前的1∶1.5∶1改变为3∶4∶3,n-6脂肪酸∶n-3脂肪酸为4∶1。这样推荐的一个原因是在日本,实践MUFA摄入比为SFA和PUFA的1.5倍的饮食标准是困难的。因此,在脂质的脂肪酸组合物中,提高了MUFA含量。单价不饱和脂肪酸油酸混合到脂肪酸组合物中,其在混合物中的含量超过30%,优选30-60%。含有大量油酸的脂质来源包括富含油酸的向日葵油、油菜籽油、橄榄油、富含油酸的红花油、大豆油、谷物油和棕榈油。此外,经营养调整的油和脂肪(NOF公司)也是一种含油酸的脂质原料。可以使用向日葵油、油菜籽油、橄榄油和含橄榄油的混合物。每100g产品中适宜的油酸含量为1-6g。另外,添加多价不饱和脂肪酸如DHA、EPA、花生四烯酸、以及中等链长的脂肪酸如辛酸、癸酸、月桂酸来调整SFA∶MUFA∶PUFA至3∶4∶3。
3.碳水化合物和食用纤维
本发明所涉及的主要碳水化合物是帕拉金糖。其他碳水化合物的例子包括糖醇(山梨糖醇、木糖醇、麦芽糖醇(maltitol)等)、蜂蜜、砂糖、葡萄糖、果糖和转化糖。
帕拉金糖包括帕拉金糖浆、还原性帕拉金糖或帕拉金糖淀粉糖浆。帕拉金糖淀粉糖浆是一种淀粉糖浆形式的液体物质,其含有的主要成分为帕拉金糖脱水聚合时产生的低聚糖如四糖、六糖和十糖。与蔗糖类似,帕拉金糖消化为葡萄糖和果糖后被吸收(Goda,T.等,Journal of Japanese Societyof Nutrition and Food Science,Vol.36(3):169-173,1983)。然而,由于帕拉金糖水解速度缓慢,只有蔗糖的1/5(Tsuji,Y.et al.,J.Nutr.Sci.Vitaminol.,32:93-100,1986),因而其被摄入后血液中葡萄糖和胰岛素的浓度长时间保持在一个稳定的水平(Kawai,K.etal.,Endocrinol,Japan,32(6):933-936,1985)。
每100mL产品中帕拉金糖的含量可以为4-15g,优选5-6g。
蛋白质、脂类和碳水化合物的能量比率与“第6版日本人能量需求”中基本相同,认为蛋白质为15-25千卡,脂类为20-30千卡,碳水化合物为45-65千卡。
食用纤维可以分为水溶性食用纤维和不溶性食用纤维。不可吸收的低聚糖、乳糖、乳糖醇(lactitol)或棉子糖可用作水溶性食用纤维。不可吸收的低聚糖未经消化就到达大肠,使肠道双歧杆菌活化并生长,从而改善肠道环境。乳糖是由半乳糖和果糖组成的合成二糖,用作治疗高氨血症的基础药物制剂(Bircher,J.et al.,Lancet:890,1965)。起因于慢性肝衰的慢性复发性肝性脑病对乳糖治疗、灌输肝衰特异性氨基酸(Fischer溶液)等治疗反应良好。乳糖醇(β-半乳糖基-山梨糖醇)被认为是第二代半乳糖基果糖(lactulose),具有与半乳糖基果糖相似的临床效果(Lanthier,PL.and Morgan,M.,Gut,26:415,1985;Uribe,M.,等,Dig.Dis.Sci.,32:1345,1987;Heredia,D.等,J.Hepatol,7:106,1988;Riggio,O.,等,Dig.Dis.Sci.,34:823,1989),目前被用作高氨血症的治疗剂。
其他候选水溶性食用纤维包括改善脂类代谢(降解胆固醇和甘油三酯)的产品如果胶(原果胶、果胶酯酸、果胶酸)、瓜尔豆胶(guar gum)酶降解产物和罗望子(tamarind)胶。瓜尔豆胶降解产物抑制血液葡萄糖水平的升高和胰岛素的减少(Yamatoya,K.等,Journal of Japanese Society of Nutrition andFood Science,Vol.46:199,1993)。此外,候选水溶性食用纤维还包括高分子量水溶性食用纤维:魔芋(konjac)葡甘露聚糖、褐藻酸、低分子量褐藻酸、psyllium、阿拉伯树胶、海藻多聚糖(纤维素、木质素样物质、琼脂、角叉胶、褐藻酸、fucodine和昆布多糖)、微生物产生的胶(威伦胶(welan gum)、可德胶(curdlan)、黄原胶、gellan胶、葡聚糖、短梗霉多糖(pullulan)和拉姆珊(rhamsan)胶)、其他树胶(种子来源的刺槐豆(locust bean)胶、罗望子胶、塔拉(tara)胶、来自汁液的刺梧桐(karaya)树胶和西黄蓍胶);低分子量的水溶性食用纤维:葡聚糖、不吸收的糊精、麦芽糖醇等。
不溶性食用纤维增加大肠中未消化物质的量且缩短其通过时间。这增加了通便频率和大便量。候选不溶性食用纤维的例子包括纤维素、半纤维素、木质素、壳多糖、脱乙酰壳多糖、大豆食用纤维、麦麸、松木纤维、谷物纤维和甜菜纤维。
4.维生素
目前已知的维生素有13种。其中,已知维生素A、K、和维生素B复合体(B1、B2、烟酸、B6、泛酸、叶酸、B12和生物素)与肝密切相关。与肝病的主要关系是维生素A的缺乏与过量、维生素B复合体的缺乏和维生素K的过量。
当阻塞性黄疸或类似疾病导致肠道胆汁不足时,维生素A吸收速率降低、导致维生素A缺乏。此处,在低蛋白营养条件下,维生素A结合蛋白(RBP)生产减少。这样,维生素A没有被运送到目标器官、维生素A缺乏症状就表现出来了。在代偿失调性肝硬化中,维生素A稍微过量就表现出中毒症状。在慢性肝病中可观察到维生素B复合体的利用发生紊乱。由于肠细菌合成的维生素K也可以被利用,因而维生素K缺乏现象不常见。然而,当由于阻塞性黄疸导致肠道胆汁不足时会导致维生素K吸收速率降低。
因此,基于上述维生素与肝的关系,本发明的营养组合物可以包括适当量的每种维生素。
5.矿物质
在体液调节中通常讨论的电解质为钠、氯、钾、磷、钙和镁。当制备矿物质配方时需考虑三种个因素:(1)摄入细胞的矿物质是否供应充足;(2)病人的内分泌环境是否足以应付所服用的各类营养物质及其用量;和(3)所给予的水的量是否足够用于测量肾的渗透负荷,是否足够用于维持适当的尿渗透压。
也可以包括铁和天然来源的痕量元素如矿物酵母如铜酵母、锌酵母、硒酵母、锰酵母和铬酵母。葡萄糖酸铜、葡萄糖酸锌等也可以使用。
所述营养组合物具有约300-1000mOsm/L的渗透压,如约300-750mOsm/L的渗透压。室温测量时,所述营养组合物具有约5-40cp(1cp=0.001Pa?s),或者优选低于20的粘性。
所述营养组合物的热量为大约1-2千卡/ml,或者优选1-1.5千卡/ml。
所述营养组合物优选为直接可用形式。这种形式的营养组合物可以使用一管子从鼻子给药直至胃和空肠(小肠的一部分),或者口服摄入。这样的营养组合物可以采用不同的形式,例如,果汁或奶昔型饮料。所述营养组合物也可以是临用前重配的可溶性粉末。
所述营养组合物可以含有不同的香料(如,香草)、甜味剂和其他添加物。可以使用人造甜味剂如天冬苯丙二肽酯(aspartame)。
此外,可以添加5mg至500mg(0.005%至0.5%)的食用伞菌提取物以减小排泄物的气味,添加10μg至200μg(0.00001%至0.0002%)类胡萝卜素类物质(如,α-胡萝卜素、β-胡萝卜素、番茄色素(licopine)和叶黄素)用于营养强化。
另外,儿茶酚、多酚之类也可以作为抗氧化剂包括在内。
营养组合物可以通过如表3所示的将蛋白质、碳水化合物和脂类混合在一起来制备。此时,可以在混合物中放入乳化剂。
本发明的营养组合物的制备可以采用本领域熟知的方法来进行。例如,这些方法包括,液体营养组合物的预热杀菌,然后在无菌条件下将其填充到容器中(例如,既使用UHT杀菌又使用无菌包装的方法),或者将液体营养组合物注入容器,然后对容器加热灭菌(例如,使用高压灭菌器)。
当本发明的营养组合物以液体形式使用时,可以将均匀的物质注入一个罐状的容器中,然后压热(retort)灭菌,或者可选地约140-145℃加热约5-8秒再次灭菌、冷却,然后无菌填充。当以粉末形式使用时,均匀的物质可以例如喷雾干燥。
本发明的营养组合物可以用作食物对急性肝炎(暴发型肝炎)、慢性肝炎、代偿性肝硬化和代偿失调型肝硬化进行营养调控。本发明的营养组合物尤其可用于对有可能发展为肝性脑病的慢性肝衰进行营养调控。尤其是,本发明营养组合物可用来对能摄入食物的慢性肝衰患者进行营养补充。
此外,本发明的营养组合物可用于为遭受外界刺激如手术、感染和烫伤的患者进行营养调控。
本发明的营养组合物可用作肝病患者的治疗性食物(肝病饮食),或者插管或肠道输入的营养组合物。
给予患者营养组合物依赖于病人的身体状况、体重、年龄以及所述营养组合物是否唯一的营养来源。由主管医师决定给予量。
附图简述
图1是乳清分离物(WPI)水解产物的UF滤过液(截止分子量:10,000)的反相层析。
图2显示在半乳糖胺肝病模型大鼠中营养组合物和Meibalance C对GOT和GPT升高的抑制效应。
图3显示给予半乳糖胺后血液GOT和GPT浓度的变化。
图4显示给予ConA后血液GOT浓度的变化。
图5显示给予ConA后血液GPT浓度的变化。
图6显示给予ConA后血液TNF-α浓度的变化。
图7显示乳清蛋白水解产物对抑制LPS诱导的TNF-α生产的影响。
图8显示乳清蛋白水解产物对抑制IL-6生产的影响。
图9显示乳清蛋白水解产物剂量对抑制LPS诱导的TNF-α生产的影响。
实施本发明的最佳方式
下面将参考实施例和试验例详细解释本发明,但不能将其理解为对本发明的限制。
[实施例1]乳清蛋白水解产物的制备
将含有约90%干蛋白的乳清蛋白分离物(WPI,Davisco)溶于蒸馏水中得到浓度为8%(w/v)的蛋白溶液。将溶液85℃加热2分钟使蛋白质变性。加热之后溶液的pH值大约为7.5。加入相对于底物浓度为2.0%的Alcalase(酶,Novozymes)2.4L进行水解,此混合物于55℃反应3小时。加入相对于底物浓度为3.0%的猪源胰蛋白酶PTN 6.0S(Novozymes Japan),55℃反应3小时。完全水解用时6小时。反应完成时的pH值为约7.0。离心乳清蛋白水解产物(20,000×g,10min),然后用分级分子量为10,000的UF膜(Millipore,Ultrafree-MC)过滤。
滤出液进行反相HPLC层析(层析谱见图1)。
条件
样品:乳清蛋白水解产物UF滤液
柱:C18SG120(Shiseido)4.6mmΦ×250mm
洗脱液:A;0.1%三氟乙酸水溶液/乙腈 5/95
B;0.1%三氟乙酸水溶液/乙腈 32/68
A——>B 60分钟线性浓度梯度
流速:1mL/min
检测:215nm(UV/可视检测器)
[实施例2]营养组合物的制备
使用标准方法制备含有表3成分的营养组合物。使用实施例1中制备的乳清蛋白水解产物。可以从Shin Mitsui Sugar Co.获得帕拉金糖,从NOF公司获得新制备的油和脂肪。奶源磷脂可由如JP-A Hei7-173182的方法获得。示例如下:
将2000mL 99.5%的乙醇加至800g的缓冲血清(BAEF)(Corman),搅动5小时,然后吸滤。滤出液减压浓缩得到160g粗脂。将480mL丙酮加至粗脂,混合物搅动0.5小时然后吸滤。480mL丙酮加至滤渣,混合物搅动0.5小时然后吸滤,将滤渣真空干燥得到50g磷脂浓缩物。
表3
制得的油和脂肪包含93%的高油酸向日葵油和7%紫苏(perila)油,n-6/n-3为1.54。此组合物列于表4。
表4
脂肪酸 | %含量 |
饱和脂肪酸油酸亚油酸亚麻酸 | 7.680.06.44.2 |
奶源磷脂组合物列于表5。
表5
磷脂 | % |
磷脂酰胆碱磷脂酰乙醇胺鞘磷脂 | 24.220.417.1 |
[试验例la]半乳糖胺肝病抑制效应(1)
测定了本发明的营养组合物和作为对照的Meibalance C的抑制大鼠半乳糖胺肝病的能力。Meibalance C[Meiji Dairies Corp.]是—种半消化形式的全营养流体食品。
材料与方法
雄性Sprague-Dawley大鼠(六周龄,日本SLC)先饲养一周,然后根据体重分为两组:一组用表3所示的营养组合物喂养(n=8);另外一组用Meibalance C喂养(n=8)。
将D-半乳糖胺?HCl(Wako Pure Chemicals)溶于生理盐水至200mg/mL,然后以300mg/kg的剂量腹腔内给予每组大鼠。这一天视为第0天。给予后,鼠的食物变为营养组合物或Meibalance C。第7天,以600mg/kg的剂量腹腔内给予每组鼠半乳糖胺盐酸。第9天,禁食4小时后二乙基乙醚麻醉,从腹大动脉取血。离心(3,000rpm,10min)获取血清,然后-20℃存储直至检测(随后一天)。在收集血液的当天测量血清中氨浓度。另外,取下肝和胰称重。使用Fuji Dry Chem进行血清AST(GOT)、ALT(GPT)、总蛋白、白蛋白、氨、胆固醇、甘油三酯的生化测试。称量肝重和胰重、解剖尸体。实验期间,动物可以自由进食进水。测量体重和进食量。
生化测试结果以平均值±标准误表示。统计处理时,使用Student′s t检验得到偶数分布,使用Mann-Whitney检验获得奇数分布。显著性水平设定为5%以下。
图2显示GOT和GPT检测结果。表6对体重、进食量、肝重、胰重、总蛋白、白蛋白、氨、胆固醇和甘油三酯水平测量结果进行了总结。
表6
数据项 | Meibalance C | 营养组合物 |
体重(g)食物摄入量(g)肝重/体重×100%胰重/体重×100%《生化测试》总蛋白(g/dl)白蛋白(g/dl)氨(μg/dl)胆固醇(mg/dl)甘油三酯(mg/dl) | 249.4±2.8169.7±1.82.99±0.120.27±0.014.6±0.23.1±0.2314.9±27.432.9±2.4106.0±11.4 | 274.0±3.0<sub>*</sub>168.5±6.94.13±0.09<sub>*</sub>0.22±0.01<sub>*</sub>5.8±0.1<sub>*</sub>3.7±0.1<sub>*</sub>177.0±21.2<sub>*</sub>63.8±2.6<sub>*</sub>79.4±8.2<sub>*</sub> |
*p<0.05
如图2所示,在半乳糖胺肝病模型中,取食Meibalance C的组血清GOT和GPT水平升高,而取食营养组合物的组被显著抑制。另外,营养组合物组的血清总蛋白、白蛋白、胆固醇和甘油三酯水平相对于Meibalance C组显著升高,而氨水平被显著(p<0.05)抑制。
虽然两个组的进食量几乎相同,但与Meibalance C组相比,营养组合物组的体重、肝重和胰重显著(p<0.05)增加。
测定血清GOT和GPT活性主要是为了理解器官紊乱的程度,因为当肝细胞恶化或坏死时GOT和GPT进入血液。虽然总血清蛋白、白蛋白、胆固醇和甘油三酯水平并非必然指示相应器官的失调,但它们可以用来评估对肝功能,包括如蛋白质合成和脂类代谢等基础功能的影响。
根据这些结果,可预期本发明营养组合物对慢性肝衰的治疗是有效的。
[试验例1b]半乳糖胺肝病抑制效应(2)
六周龄Balb/c鼠(日本SLC)先用AIN-93M(oriental Yeast)饲养一周,然后根据体重分为每组8只鼠的多个组。再用Hepas(Morinaga Clinico)培养8天,将依照表7混合而得的营养组合物装入罐状容器后压热灭菌然后冻干。在饲养的第8天,将溶于PBS的D-半乳糖胺(Wako Pure Chemicals)以每kg体重400mg的剂量给予每只鼠。然后以每kg体重10μg的剂量腹腔内给予LPS(Wako Pure Chemicals)。给予后8小时从尾静脉收集血液。第二天在醚麻醉条件下从动脉收集血液。动物可以自由进食进水。离心血液分离血清,通过Fuji Dry Chem测量GOT和GPT。以平均值±标准误差表示结果,使用Mann-Whitney检验(*:p<0.05)来进行差异显著性测定。
表7用于肝病的流体食物组合物
来源 | 成分 | 每100mL含量 | 单位 |
乳清蛋白水解产物NFL夸克 | 乳清肽夸克 | 1.833.74 | gg |
帕拉金糖NSD700 | 帕拉金糖麦芽糖糊精 | 6.156.40 | gg |
松树纤维C | 不消化糊精 | 0.73 | g |
增稠剂 | 果胶 | 0.80 | g |
新制备的油和脂肪卵磷脂F(大豆油) | 油酸磷脂 | 2.5970.133 | gg |
维生素A-50油维生素AD油天然维生素EThamine盐酸维生素B6盐酸(V.B6)烟酰胺(烟酸)泛酸钙核黄素(V.B2)维生素B12(V.B12)水溶性复合类胡罗卜素叶酸L-抗坏血酸钠(V.Can) | 维生素A维生素D维生素E维生素B1维生素B6烟酸维生素B2维生素B12胡罗卜素维生素C | 0.110.5616.260.2920.4592.420.8540.2351.140.4267580.8 | mgmgmgmgmgmgmgmgμgmgμgmg |
磷酸钾氯化钠乳酸钙氯化镁柠檬酸硫酸亚铁碳酸氢钠 | 钾钠钙镁铁 | 0.1450.11260.58240.04260.350.004540.1125 | ggggggg |
目前,Hepas是唯一可在市场上得到的用于肝病的流体食物。将Hepas的效果与依照表7的组合物制备的用于肝病的流体食物的效果进行比较。将半乳糖胺和LPS腹腔内给予小鼠,8小时和24小时后测定GOT和GPT的水平。如图3所示,Hepas使GOT和GPT升高,引发肝炎。另一方面,与Hepas相比,本发明用于肝病的流体食物明显抑制GOT和GPT的升高。
上述结果中,没有观察到Hepas对肝炎的抑制效应。另一方面,在半乳糖胺/LPS诱导的鼠肝炎模型中,可以确定本发明的治疗肝病的流体食物对于抑制肝炎是有效的。
[试验例1c]病毒性和自身免疫性肝病抑制效应
六周龄Balb/c鼠(日本SLC)先用AIN-93M(oriental Yeast)饲养一周,然后根据体重分为每组10只鼠的多个组。然后其食物改为WPI(Davisco),或者改为实验食物,其中AIN-93M(含14%酪蛋白)的酪蛋白被实施例1中制备的乳清蛋白水解产物取代,致使乳清蛋白水解产物的含量为食物蛋白含量的25%和50%。将鼠饲养14天。在第14天,以每kg体重15mg的剂量静脉注射溶于PBS的ConA(Sigma)。注射后2、4和8小时从尾静脉收集血液。第二天在麻醉状态下,从动脉收集血液。动物可以自由进食进水。离心血液分离血清,用Fuji Dry Chem测量GOT和GPT。用ELISA(Amersham Bioscience)测定TNF-α细胞因子水平。以平均值±标准误差表示结果,使用Mann-Whitney氏U检验(*:p<0.05)来进行差异显著性测定。
在酪蛋白组,肝炎的指示物质GOT和GPT在给予ConA后8至24小时升高。另一方面,在WPI和乳清蛋白水解产物组,GOT和GPT的升高被显著抑制(图4和5)。确认25%乳清蛋白水解产物组显示与50%WPI组等同或更强的效应。因此,预期源于WPI的乳清蛋白水解产物具有比WPI更强的效应。也同时测定了这些相同个体中细胞因子的生产。在酪蛋白组,血清TNF-α浓度在给予ConA后两小时升高,4小时后降低(图6)。给予ConA后两小时,WPI组和乳清蛋白水解产物组的TNF-α浓度显著低于酪蛋白组。证实WPI和乳清蛋白水解产物对抑制TNF-α的分泌是有效的。抑制细胞因子的生产也可以抑制肝炎的诱发,并因此抑制GOT和GPT的升高。如上所述,在ConA诱导的肝病模型中,证实WPI来源的乳清蛋白水解产物可抑制肝病。
[试验例2]乳清蛋白水解产物的抗炎效应
<方法>
六周龄雄性ICR鼠(日本SLC)饲养一周,然后分成每组6只鼠的三个组,每组的平均体重相同。通过向纯化食物(AIN-93M)中添加按重量计算14%的如下成分制得的实验食物作为蛋白来源:10%酪蛋白(对照组)、50%酪蛋白+50%WPI(Davisco Foods)、或50%酪蛋白+50%乳清蛋白水解产物(实施例1中制备的)。然后将小鼠饲养7天。
饲养后,以1.4μg/g体重的剂量腹腔内给予脂多糖(LPS)。90分钟后从眼窝取血,离心(10,000×g,15分钟)得到血清。用ELISA试剂盒(Amershambioscience)测定血清TNF-α和IL-6。用Fisher氏PLSD检验组间差异显著性。血清TNF-α浓度和IL-6浓度分别如图7和图8所示。
<结果>
与酪蛋白组(对照组)相比,WPI组在给予LPS后TNF-α的生产趋向于被抑制,而在乳清蛋白水解产物组中被显著抑制(p=0.033)(图7)。
与酪蛋白组(对照组)相比,WPI组在给予LPS后IL-6的生产也趋向于被抑制,而在乳清蛋白水解产物组中被显著抑制(p=0.0002)(图8)。
上述结果显示,口服乳清蛋白水解产物后,由LPS刺激的TNF-α和IL-6的生产被显著抑制。通过改变乳清蛋白的含量进一步检测到这样的TNF-α生产抑制。
更特别地,以100%酪蛋白、80%酪蛋白+20%乳清蛋白水解产物、70%酪蛋白+30%乳清蛋白水解产物、以及50%酪蛋白+50%乳清蛋白水解产物作为蛋白质来源做了一些相似的实验。经F检验后,用Bonferroni/Dunn检验证实组间差异显著性。这些结果列于图9。
与酪蛋白组相比,20%乳清蛋白水解产物组中给予LPS后的TNF-α生产趋向于被抑制,而在30%和50%乳清蛋白水解产物组中被显著抑制(p=0.0496和p=0.0479)。
<讨论>
1.关于肝病和TNF-α之间的关系
在炎症和免疫反应期间,TNF-α、IL-1和IL-6主要在巨噬细胞和内皮细胞中生产,作为致热原发挥功能,也直接对肝细胞起作用以促进产生急性期蛋白(acute phase proteins)(C-反应蛋白;CRP)(Hepatology 23:909-916,1996;J.Immunol.,146:3032-3037,1991;Intensive Care Med.,24:224-229,1998;Hepatology 9:497-499,1989)。
急性肝炎(尤其是爆发性肝炎)和酒精性肝损害中,炎症细胞因子的介入表现为发烧、白细胞增多、CRP阳性等。
TNF-α在内毒素刺激后由巨噬细胞生产,可以引起多种器官障碍(″Hepatic Failure-Fundamental and Clinical″,Japan Nedical Journal,Tokyo,1994,pp.30-46;″Hepatic Failure-Fundamental and Clinical″,Japan MedicalJournal,Tokyo,1994,pp.123-137)。事实上,在暴发型肝炎患者中,网状内皮系统的功能降低、也时常可以观测到高内毒素血症的连续出现。因此认为TNF-α和IL-1的生产在体内得到推动(Lancet,2:72-74,1988)。与急性肝炎相比,暴发型肝炎患者血液中大多数炎症细胞因子的浓度显著上升,尤其是,TNF-α和IL-6的浓度与人肝细胞生长因子(HGF)高度相关,HGF是肝再生的指标(Clin.Exp.Immunol.,98:71-77,1994)。
另一方面,作为慢性肝病的肝硬化的患者血液中炎症细胞因子的浓度显著高于未发生肝硬化的患者。不考虑疾病的原因,这反映的是肝功能紊乱而非炎症(Gastroenterology,103:264-274,1992)。在慢性乙型肝炎患者中,IL-1的生产增强并与肝纤维化程度相关,据报道IL-1在肝硬化进程中是重要的(Gastroenterology,94:999-1005,1988)。
关于肝病和IL-6之间的关系
在酒精性肝硬化中,IL-6血液水平的升高和外周血单核细胞中IL-6的生产与IgA水平正相关,与IL-2和IFN-γ的生产负相关(Clin.Exp.Immunol.,77:221-225,1989)。血液IL-6的活性在慢性肝炎急剧恶化期间也有所升高(Am.J.Gastroenterol.,86:1804-1808,1991)。IL-6血液水平以及未经刺激的外周血单核细胞产生IL-6被认为反映个体肝脏炎症的程度。
急性病毒性肝炎中,在窦状小管内皮细胞、枯否(Kupffer)细胞和侵入性单核细胞中探测到了IL-6(J.Clin.Pathol.,45:408-411,1992)。慢性肝炎中,IL-6主要在侵入性淋巴细胞和门静脉区成纤维细胞中被探测到。因此,在急慢性肝病中,预期IL-6的表达与炎症和免疫反应紧密相关,此时不考虑这些疾病的病因。IL-6促进肝细胞再生,其过量生产可能引起组织损伤和纤维化。
2.营养给予途径和细胞因子的生产
在外来刺激期间,为阻止细胞因子引起的代谢和器官功能紊乱,诱导细胞因子在局部的正常生产并阻止其向全身扩散是可能是合理的。因此,考虑到在外来刺激时改变细胞因子生产的可能性,讨论了不同营养给予方法之间的差异。对于未遭受外来刺激的健康成年人,肠或静脉内给予营养一周不会导致出现TNF和IL-6血液水平的明显差异(New Horizon,2:164-174,1994)。然而据报道,当对健康成年人提供肠或静脉内营养7天后静脉注射内毒素时,就所引起的全身性生物反应如发烧以及TNF和应激性激素的释放而言,肠营养要比静脉营养轻微(Ann.Surg.,210:449-457,1989)。Saito等也对鼠由肠途径给予细菌并经不同途径给予营养来研究营养给予途径和细胞因子生产之间的关系。其结果证实通过肠营养来改变细胞因子的生产在生物反应方面比静脉营养更加有利(Ann.Surg.,223:84-93,1996)。
3.关于营养组合物和肝病抑制效应之间的关系
当本发明的营养组合物被口服摄入时,内毒素诱导的TNF-α和IL-6在血液中浓度的升高被显著抑制。此抑制效应主要归因于营养组合物中所含的乳清蛋白水解产物。血液TNF-α和IL-6浓度升高的抑制可能归因于TNF-α和IL-6生产的改变,此改变的发生是由于营养组合物的口服摄入。
工业实用性
本发明的营养组合物可用于急性肝炎(暴发型肝炎)、慢性肝炎、代偿性肝硬化、代偿失调性肝硬化的营养调控。本发明的尤其可用于有发展为肝性脑病的慢性肝衰。在慢性肝衰中,如果能够摄取食物,标准是限制蛋白质摄入量。然而,当较高程度的蛋白质限制持续一个较长的时间时,食欲降低,蛋白质分解代谢增强,营养匮乏状况加剧。因此,多少有些营养补充是必要的。每餐都补充一些本发明的食物型营养组合物可以改善慢性肝衰病人的营养状况。
此外,本发明的营养组合物还可用来对经历手术、感染、烫伤等外来刺激的病人进行营养调控。
Claims (7)
1.一种用于肝病患者或用于遭受强烈外来刺激的病人的营养组合物,包含:每100mL该组合物中0.9-3g奶蛋白水解产物和每100mL该组合物中2-6g源于发酵奶的蛋白质,作为蛋白质成分;富含油酸的油和每100mL该组合物中0.1-0.5g奶卵磷脂和/或大豆卵磷脂,作为脂类成分,其中富含油酸的油中油酸的含量为占总脂肪酸组成的30%以上、且每100g该组合物中有1-6g油酸;每100mL该组合物中4-15g帕拉金糖,作为碳水化合物成分。
2.权利要求1的营养组合物,其中所述的奶蛋白选自由酪蛋白、奶蛋白浓缩物、乳清蛋白浓缩物、乳清蛋白分离物,α-乳清蛋白、β-乳球蛋白、和乳铁蛋白所组成的组中的蛋白。
3.权利要求1的营养组合物,其中所述的源于发酵奶的蛋白质源于发酵奶中乳清减少的组合物。
4.权利要求1的营养组合物,其中所述的源于发酵奶的蛋白质源于新鲜干酪。
5.权利要求4的营养组合物,其中所述的新鲜干酪是夸克。
6.权利要求1的营养组合物,其中所述的奶蛋白水解产物通过用源于地衣芽孢杆菌的alkalase和源于猪胰腺的胰蛋白酶来水解乳清蛋白分离物而获得。
7.权利要求6的营养组合物,其中所述的奶蛋白水解产物是一种使用分级分子量为10,000的超滤膜进一步处理而获得的滤过液。
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CN103957720B (zh) * | 2011-11-30 | 2016-05-25 | 株式会社明治 | 肠内菌群改善用营养组合物 |
Also Published As
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TW200412990A (en) | 2004-08-01 |
HK1083174A1 (en) | 2006-06-30 |
DE60332760D1 (de) | 2010-07-08 |
TWI317636B (en) | 2009-12-01 |
JP2006515287A (ja) | 2006-05-25 |
JP2013136602A (ja) | 2013-07-11 |
US20090233865A1 (en) | 2009-09-17 |
US7563458B2 (en) | 2009-07-21 |
WO2004047566A1 (en) | 2004-06-10 |
JP2011006425A (ja) | 2011-01-13 |
AR042107A1 (es) | 2005-06-08 |
CN1741749A (zh) | 2006-03-01 |
US8778404B2 (en) | 2014-07-15 |
ES2344640T3 (es) | 2010-09-02 |
ATE468762T1 (de) | 2010-06-15 |
NZ540775A (en) | 2007-08-31 |
BR0316512A (pt) | 2005-10-04 |
AU2003283831A1 (en) | 2004-06-18 |
MY169519A (en) | 2019-04-22 |
EP1575379A1 (en) | 2005-09-21 |
CA2506603C (en) | 2011-06-28 |
KR101038354B1 (ko) | 2011-06-01 |
CA2506603A1 (en) | 2004-06-10 |
DK1575379T3 (da) | 2010-09-13 |
EP1575379B1 (en) | 2010-05-26 |
KR20050083950A (ko) | 2005-08-26 |
JP5688818B2 (ja) | 2015-03-25 |
US20060073186A1 (en) | 2006-04-06 |
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