奶牛酮病研究进展
奶牛酮病检测方法的比较和牛乳、血清中β-羟丁酸相关性研究
奶牛酮病检测方法的比较和牛乳、血清中β-羟丁酸相关性研究奶牛酮病是一种常见的疾病，对奶牛的生产和健康产生负面影响。
因此，及早检测和诊断奶牛是否患有酮病非常重要。
本文旨在比较奶牛酮病检测方法，并探讨牛乳和血清中β-羟丁酸的相关性研究。
奶牛酮病是由于葡萄糖代谢紊乱引起的一种代谢性疾病。
当奶牛在过渡期（产后的几周内）时，其摄入的能量不足以满足产奶的需求，因此身体会开始从体内脂肪储备中分解脂肪产生能量。
然而，这个过程会导致体内酮体（主要是β-羟丁酸）积累过多，从而引发酮病。
目前，常见的奶牛酮病检测方法主要包括尿液检测、血液检测和牛乳检测。
尿液检测是一种简单和快速的方法，可以通过检测尿液中的酮体含量来判断奶牛是否患有酮病。
然而，尿液检测存在一定的局限性，因为尿液中的酮体浓度与血液中的酮体浓度之间存在一定的差异。
血液检测是一种准确性较高的方法，可以直接测量血液中的β-羟丁酸浓度。
然而，血液检测需要采集血液样本，并且需要专业的实验室设备进行分析。
这种方法对兽医的要求较高，也增加了检测的成本。
牛乳检测是一种相对较新的检测方法，可以通过测量奶牛产奶时的乳液中的β-羟丁酸浓度来判断是否患有酮病。
与血液检测相比，牛乳检测具有便捷性和实用性的优势。
牛农可以直接在奶牛产奶时采集乳液样本，并使用便携式检测设备进行分析。
近年来，一些研究还发现了牛乳和血清中β-羟丁酸的相关性。
他们发现，在奶牛产奶前后，牛乳和血清中的β-羟丁酸浓度存在一定的相关性。
这一发现表明，可以通过检测牛乳中的β-羟丁酸浓度来评估奶牛是否患有酮病，并进行相应的干预措施。
总结来说，各种奶牛酮病检测方法各有优劣。
尿液检测简单快速，但准确性较低。
血液检测准确性高，但需要专业设备和操作。
牛乳检测具有便捷性和实用性，可以在奶牛产奶时进行监测。
牛乳和血清中的β-羟丁酸具有一定的相关性，可以作为评估奶牛酮病的依据。
未来的研究还需进一步完善、验证和推广这些检测方法，以提高奶牛酮病的预防和管理水平综上所述，牛乳检测作为一种便捷且实用的方法，可以用于评估奶牛是否患有酮病。
奶牛酮病及其研究进展
生酮病后治疗费用高 ，产奶量大幅度降低 ，乳成分 改变 ，繁殖率降低及淘汰率升高 ，而亚临床酮病发
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使患其他疾病的概率增加 ，可能是高酮血症损害了
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谓的“ 最好的药物是营养平衡的饲料” 。
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一
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维普资讯
的发 生 与产褥 热 、真 胃移 位 、脂 肪肝 等疾 病 的发 生
有 密切 的关 系 ，产褥热 、真 胃移位 、脂 肪肝 的发 生 ｉ 定汉 等研 究 发现 ，在 ５ Ｏ头 左侧 真 胃移 位 的奶 牛
其 次酮 病 的发 生 与乳 房 炎 、子宫 炎 、产 褥 热 、
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周 ，奶 牛亚临床酮病发病率达 ５％。如美 国乳牛 ９ 酮 病 发 病 率 为 ５ ％ ，而 印度 １．９ ，其 他 如 荷 ． ０ ４６％
用 约 １０ ０元 ，而用 高锰 酸钾 则 只需 约Ｏ６ ６． ０ ． ０元 ，故 用 高锰 酸钾 治疗 酮体 阳性 牛 既经 济 又实惠
奶牛酮病的最新疗法
免疫疗法
主动免疫
利用抗原（病原体或疫苗）刺激机体产生特异性免疫反应，从而增强机体免疫力。对于奶牛酮病，可 以通过注射疫苗来提高奶牛的免疫力。
被动免疫
利用抗体或细胞因子等免疫活性物质来增强机体免疫力。例如，给病牛注射抗酮抗体或细胞因子等。
基因治疗
• 基因治疗是指利用基因工程技术将外源基因导入受体细胞，以 纠正或补偿因基因缺陷引起的疾病。目前，在奶牛酮病的治疗 中，基因治疗尚处于实验室研究阶段，尚未应用于临床。
临床效果评估
治愈率：最新疗法二的治愈率达到了85%左右，相比传 统疗法有显著提高。
操作简便：相比传统疗法，最新疗法二的操作更为简便 ，易于在基层推广。
最新疗法二：具体效果
创新性：最新疗法二是一种创新性的治疗方法，利用了 最新的科研成果，为奶牛酮病的治疗提供了新的思路。
畜牧业前景展望
奶牛产业的发展
供了良好的前景。
未来研究方向建议
01
02
03
深入研究病因
针对奶牛酮病的病因进行 深入研究，以便更好地预 防和治疗此病。
探索新的治疗方法
积极探索新的治疗方法， 寻找更有效、更安全的治 疗方案。
提高诊断技术
不断提高奶牛酮病的诊断 技术，以便更早地发现和 治疗此病。
06
结论与参考文献
结论回顾
酮病是奶牛常见的代谢性疾病，主要表 现为酮血、酮尿、食欲减退等症状，对 奶牛的健康和生产性能产生负面影响。
染。
中西药结合制剂
穿心莲内酯滴丸
该药物由中药穿心莲提取物与西药潘生丁合成，具有 清热解毒、抗菌消炎、抗血小板聚集等多重作用，可 用于治疗奶牛的细菌感染和预防血栓形成。
复方丹参注射液
该药物由中药丹参提取物与西药双嘧达莫合成，具有 活血化瘀、抗菌消炎、抗血小板聚集等多重作用，可 用于治疗奶牛的细菌感染和预防血栓形成。
奶牛酮病的研究综述
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１ 病 因
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较 为 复 杂 。 根 据 发 生 原 因 可 以 分 为 生
产 性 酮 病 、继 发 性 酮 病 、食 源 性 酮 病 、 饥 饿 性 酮 病 和 由于 特 殊 营 养 缺 乏 引 起 的 营 养 性 酮 病 。 生 产 性 酮 病 发 生 在 体 况 极 好 ，泌 乳 能 力 强 ．饲 料 质 量 高 的 母 牛 ： 继 发 性 酮 病 是 因 某 些 疾 病 ． 比 如 ， 奶 牛 真 胃变 位 、 创 伤 性 网 胃 炎 、
奶牛酮病早期预警技术的研究进展
奶牛酮病早期预警技术的研究进展
杜振隆;罗正中;周涛;曹随忠;严作廷
【期刊名称】《中国畜牧杂志》
【年(卷),期】2024(60)1
【摘要】近年来,奶牛养殖业进入快速发展时期,而养殖高成本、高发病率和低产出是阻碍奶牛养殖业持续发展的障碍。
其中,奶牛酮病的发病率有逐年升高趋势,不同
的胎次、产后天数、月份、泌乳量等风险因素均影响奶牛酮病的发生。
目前,基于
奶牛行为、奶牛生产性能测定数据、代谢组学技术和机器学习的酮病早期预警技术已经取得巨大进展。
本文综述了奶牛酮病的发病规律和酮病早期预警技术,为奶牛
围产期健康管理提供理论参考,对促进奶业提质增效、提高奶牛福利具有重要意义。
【总页数】5页(P31-35)
【作者】杜振隆;罗正中;周涛;曹随忠;严作廷
【作者单位】中国农业科学院兰州畜牧与兽药研究所;四川农业大学动物医学院【正文语种】中文
【中图分类】S823.1
【相关文献】
1.奶牛酮病早期监控技术的效果
2.基于DHI的奶牛酮病监测、预警及早期防控技
术体系的建立与应用效果3.奶牛体况与血浆生化指标对酮病的风险预警4.奶牛乳
与血液中酮病预警新指标的研究5.奶牛酮病监测、预警及诊治措施
因版权原因，仅展示原文概要，查看原文内容请购买。
奶牛酮病防治的研究进展
科研 ◎畜牧 善罡
奶牛酮 病防治 的研 究进展
克 里木 － 玉素甫
（ 新 疆 喀 什 地 区 巴 楚 县 英 吾 斯 塘 乡 兽 医 站 ，新 疆 巴 楚 ８ ４ ３ ８ ９ ９）
【 摘 要】 近年 来 ，随着我 国奶 牛饲 养数 量 的不 断增加 和奶 牛产 量 的持 续提 高，奶牛 酮病 的发病 率也 逐渐 增长 ，至今 已高 达２ ５ ％ｖ Ｘ 上 。 酮病 的感 染不仅 危 害 了奶 牛 的身体 健康 ，同时也 严 重影响 了奶 牛业 的稳 定发展 ， 因此 ，要 加 强对奶 牛 的科 学管 理 ，对 感染 酮病 的奶 牛要 采取 及 时治疗 。本 文主 要针 对奶 牛 酮病 的防 治进 行相 关讨 论 ，研 究 了酮病 感 染的病 因与症 状 ，并提
、
行 。同时 ， 应 用 糖 皮 质激 素肌 内或静脉注 射治疗 酮病效 果也 很 好。 ４ ． 补 糖治疗 ： 奶 牛之 所 以容 易患上 酮病 ， 主要 原 因是 体 内 消耗 糖分 过多 ， 引发低 血糖 。因此在 治疗 酮病 时 ， 可 采用 补糖 疗法， 即通过 静脉 注射 ５ ０ ％葡 萄糖溶 液 ５ Ｏ ０ ｍｌ ， 这 种 方法 可有 效解 决低 血糖 ， 并 且见 效快 ，对很 多奶 牛都 有明显 的治 疗效 果 。保持 每天 注射 ２次 ， 每次 ５ Ｏ Ｏ ｇ ， 持续 一段 时 间后 ， 便 可有 明显 改善 。 ５ ． 增 加产 糖 物质 疗法 ： 可 用丙 酸钠 １ ２ ｏ ～ ２ ０ ０ 克， 混饲 或 内 服， 连用 ７ — １ Ｏ天 ， 效果 明显 。 四、 预 防 １ ． 加强 饲养管 理 为了防止 奶 牛产前 过度肥 胖而 引起 的酮病 ，应 合理 控制 奶 牛的食用 量 ， 保 证奶 牛分娩 时的最 佳体 重。在奶 牛 分娩后 ， 将迎 来泌乳 高峰期 ， 同时奶牛也 伴有 食欲 下降等 产后症 状 ， 因 此， 在这一 时期 内要增加 奶牛 的食欲 和采食 量 ， 以维持 奶 牛在 产奶 时所 消耗的糖 分 。由于奶 牛产后体 质虚 弱 ， 免疫 力下 降 ， 各种应 激在影 响奶 牛的采 食行 为时 ，都有 可能 引发 酮病 。因 此， 要保 证 牛舍 的正 常温 度 ， 避免 对奶 牛产 生高 热 、 潮湿 的 刺 激性 。 ２ ． 建立 酮病监 测制度 很 多奶牛在 发病初 期 ， 由于发 病症状 不 明显 ， 往往被 饲养 人员所 忽略 ， 没有对 酮病产 生应 用的重 视 ， 导 致酮 病 的程度 由 轻度变 为重度 ， 从而 影响 了奶牛 业的健 康发 展 。因此 ， 针对酮 病 发病 初期 的不明显 症状 ， 应 建立起 日 常 酮病 监测 制度 ， 这样 才 能做 到早发 现早防 治。从 而减少奶 牛业 的经济 损失 。 五、 结 语 综上所 述 ， 近 年来 我 国奶 牛业 发展 良好 ， 并取 得 了较 好 的 经 济效益 。但在 饲养过 程 中 ， 由于缺 乏科 学管理 性 ， 导致 奶牛 极 容易 患上酮病 ， 从 而严重影 响 了奶 牛业 的健康发 展 。 奶 牛酮 病 感染 的原 因主要是 由于 在生产 前奶 牛过 度肥胖 ，或产 后营 养不足 ，在泌乳 期高 峰大 量产奶 导致体 内糖 分消 耗过 多而 引 发 酮病 。 酮病 发病期 通常在 产后 的 ６ 周内， 主要症 状有 食欲减 退、 情绪 低落或 过度 兴奋等 。 在治 疗时主 要 以补充 奶 牛体 内糖 分 为主 ，采用注 射激 素或葡 萄糖 以保证 奶 牛体 内糖 分 的正常 消 耗 。除 此之外 ，饲养 人 员还 应对 奶 牛的 日常管理 做到 科学 化、 合理 化 。 只有 这样 ， 才能 最大限 度的避免 奶牛 酮病发 作 ， 使 奶 牛产业 的发展 蓬勃 向上 。
奶牛酮病的致病机制和诊断方法研究进展
奶牛酮病的致病机制和诊断方法研究进展王世玺1，巴雅尔1，胡 亮21 巴彦淖尔市动物疫病预防控制中心，内蒙古巴彦淖尔 0150002 巴彦淖尔市农牧业科学研究所，内蒙古巴彦淖尔 015000摘 要：奶牛酮病作为我国奶牛养殖业面临的重大挑战，其高发率对养殖业的稳定发展构成威胁。
本文详细阐述了奶牛酮病的分类、危害、临床症状以及发病原因，同时对诊断技术进行了深入探讨。
奶牛酮病根据β-羟基丁酸水平分为亚临床型和临床型。
酮病对奶牛健康、产奶量、牛奶质量和繁殖性能造成严重影响，增加了牧场运营成本和风险。
其发病原因多样，包括能量代谢不平衡、围产期疾病、食源性因素、饥饿状态以及特定营养素缺乏等，与糖、脂、蛋白质代谢紊乱及激素调节密切相关。
在诊断方面，文章介绍了定性检测（酮粉法、试剂法、试纸条法）和定量检测（水杨醛比色法、分光光度法、气相色谱法）等多种方法。
本研究为奶牛酮病的有效防控提供了全面的知识基础和技术指导，有助于提升奶牛养殖业的健康管理与可持续发展。
关键词：奶牛酮病；代谢紊乱；发病机制；诊断方法文章编号：1671-4393（2024）03-0035-04 DOI:10.12377/1671-4393.24.03.070 引言奶牛饲养是我国农业重要组成部分，但酮病这一营养代谢性疾病的高发率对养殖业稳定发展造成巨大威胁。
围产后期奶牛由于体内激素水平剧烈变化、环境应激和泌乳而处于能量负平衡状态，容易引发机体的能量代谢紊乱，诱发酮病。
随着我国奶业规模化、集约化饲养模式快速发展，奶牛酮病发病率逐年上升，严重威胁奶牛健康和养殖业可持续发展。
本文详细介绍了奶牛酮病相关知识，重点讨论检测技术，为奶牛养殖业健康管理和发展提供参考。
1 奶牛酮病的分类及危害1.1 奶牛酮病的分类奶牛酮病是一种常见的代谢疾病，主要特征作者简介：王世玺（1976-），内蒙古临河人，本科，中级兽医师，研究方向为动物疫病防控；巴雅尔（1982-），男，内蒙古磴口人，蒙古族，本科，助理兽医师，研究方向为动物疫病防控； 胡 亮（1985-），男，内蒙古巴彦淖尔人，本科，兽医师，研究方向为动物疫病防控。
奶牛脂肪肝及酮病的最新研究进展(美国瑞信胆碱Reashure )
New Insights into Fatty Liver and KetosisJames K. DrackleyDepartment of Animal SciencesUniversity of Illinois at Urbana-Champaignemail: drackley@IntroductionFatty liver and ketosis are interrelated disturbances of energy metabolism that impact dairy cows during the periparturient or transition period. The syndromes can directly decrease performance and adversely impact cow well-being; in addition, they can predispose cows to infectious diseases and other metabolic disorders. Both situations have been extensively researched during the last several decades and the scientific literature is plentiful – yet the disorders continue to plague dairy farmers worldwide. While the descriptive pathology and metabolic characteristics have been thoroughly described by these research efforts, the mechanism or mechanisms that trigger clinical disease and the cellular processes responsible for the resultant pathologies have remained elusive. Moreover, optimal management strategies for minimizing incidence and impact are still debated.Given the central importance of management to minimize metabolic disorder during the transition period in determining profitability and cow well-being, the objective of this presentation is to review some key questions. What are fatty liver and ketosis and how common are they? When and how do fatty liver and ketosis develop? How do fatty liver and ketosis affect health and productivity? What nutrition and management practices predispose to fatty liver and ketosis, and how can management prevent them? The focus will be on new information and theories surrounding development and consequences of ketosis and fatty liver, with emphasis on recent findings from our research program. For additional information, readers may refer to several comprehensive reviews on various aspects of transition cow biology and management (Drackley, 1999; Drackley et al., 2001, 2005; Grummer et al., 2004; Overton and Waldron, 2004; Drackley and Andersen, 2006; Goff, 2006; Drackley and Dann, 2008). Negative Energy Balance and the Ketosis-Fatty Liver ComplexDairy cows undergo tremendous changes during the transition from late gestation to early lactation. The fundamental driver of the physiological changes is to ensure provision of adequate nutrients for the calf, both prenatally and postnatally. Dairy production has capitalized on this metabolic drive by selecting for ever-higher milk production. After parturition, nutrient demand is not able to be met through feed intake alone because the rate of dry matter intake (DMI) increase is slower than the rate of milk energy output. As a result, the magnitude of metabolic challenge faced by modern dairy cows is almost staggering. As demonstrated in Table 1, requirements for net energy of lactation (NE L) essentially double “overnight” as cows calve and commence lactation.The fact that many cows are able to meet this challenge without difficulty speaks to the fact that the metabolic adaptations necessary to support milk production are a component of thefactors being genetically selected. The nutrient and energy deficits after parturition are met by mobilization of body reserves and by decreasing nonessential use of glucose in non-mammary tissues. Metabolic adaptations are mediated by an exquisite pattern of hormonal shifts and Table 1. Calculated net energy of lactation (NE L) requirements (Mcal/d) for dairy cows and heifers 2 days before vs. 2 days after parturition (Drackley et al., 2005).1600-lb cow 1250-lb heifer Function Pre-fresh Fresh Pre-fresh Fresh Maintenance 11.2 10.1 9.3 8.5 Pregnancy 3.3 --- 2.8 --- Growth --- --- 1.9 1.7 production --- 18.7 --- 14.9 MilkTotal 14.5 28.8 14.0 25.1Calculated from NRC (2001). Assumes precalving body weight with average decreasefor calf and fluid loss at calving, milk production of 55 lb/d for cow and 45 lb/d forheifer, each containing 4% fat.factors being genetically selected. The nutrient and energy deficits after parturition are met by mobilization of body reserves and by decreasing nonessential use of glucose in non-mammary tissues. Metabolic adaptations are mediated by an exquisite pattern of hormonal shifts and changes in tissue responsiveness to those hormones. For example, growth hormone (GH) is increased around parturition and in early lactation (Grum et al., 1996), which increases responsiveness of adipose tissue to lipolytic signals such as norepinephrine and decreases sensitivity of insulin-dependent tissues to the action of insulin, whose concentration also decreases because of negative energy balance (NEB). The resulting increase of nonesterified fatty acids (NEFA) from adipose tissue are used as alternate fuels for much of the rest of the body, and are also converted by the liver to ketone bodies. The ketones serve as alternate water-soluble fuels that can replace glucose in many tissues, thus conserving glucose for milk synthesis.While a majority of cows are able to weather the metabolic challenges associated with initiation of milk synthesis, the fact that, on average, roughly 1 in 2 cows succumbs to some health problem during the transition period (Ferguson, 2001) underscores the fragility of the system. The etiology of most of the periparal health disorders is directly or indirectly associated with NEB (Drackley et al., 2005). Increasingly strong evidence indicates that clinical and subclinical ketosis and fatty livers are key underlying factors in development of other earlylactation disorders and disease (Duffield, 2000; Bobe et al., 2004), as well as impaired fertility (Rukkwamsuk et al., Walsh et al., 2007a,b).Metabolic Changes during the Transition PeriodAs calving approaches, concentrations of progesterone in blood decrease and those of estrogen remain high or increase (Grummer, 1995). The high circulating estrogen may be one factor that contributes to decreased DMI around calving (Grummer, 1993). During the last 3 wk of pregnancy, nutrient demands by the fetal calf and placenta are at their greatest (Bell, 1995). At the same time, depending on diet composition, DMI may be decreased by 10 to 30% compared with intake during the early dry period. This in itself may not be cause for alarm, as decreased food or feed intake around parturition is a common finding in many mammalian species (Friggens, 2003). Maintaining good appetites through and after calving are likely more important.Cows are unable to consume sufficient energy-yielding nutrients from voluntary DMI after calving to meet energetic requirements for milk production. Consequently, a state of NEB almost always occurs for a period of days to weeks in early lactation. Postpartal NEB clearly results from initiation of milk synthesis because mastectomy before parturition greatly blunts the increased concentration of NEFA released from adipose tissue at and after calving (Goff et al., 2002). However, the degree of NEB in individual cows is poorly related to milk production, or more correctly, milk energy secretion. The depth and duration of NEB is highly related to DMI (Zurek et al., 1995; Drackley et al., 2005), and thus factors that impact appetite and consumption of feed after calving are critical.Like most mammals, a number of physiological adaptive mechanisms are invoked to allow the cow to cope with the challenges induced by NEB. Cows mobilize stored triglycerides (TG) in adipose tissues as an energy supply for milk production and maintenance functions. Glycerol released from lipolysis is used by the liver for glucose synthesis in the pathway of gluconeogenesis. The fatty acids released circulate as NEFA and are distributed with blood flow to all body tissues (Drackley et al., 2001). When NEFA concentrations are elevated during early lactation, the mammary gland takes them up efficiently and converts them to milk fat. High milk fat concentrations, or high milk ratios of fat to protein, are useful as indicators of ketosis in dairy cows.The liver receives about 1/3 of all blood flow from the heart. Consequently, the liver is flooded with NEFA when blood concentrations increase around calving. The liver takes up NEFA in proportion to their concentration in blood. Within liver cells, NEFA can be 1) oxidized to carbon dioxide with the generation of ATP for the liver’s energy needs, 2) partially oxidized to the ketone bodies β-hydroxybutyrate (BHBA) and acetoacetate, which results in ATP for the liver and water-soluble energy sources for muscle and heart, or 3) re-converted to TG. Because ruminant animals are unable to effectively export TG out of the liver as very-low density lipoproteins, TG can accumulate and cause fatty liver. Increased ketone body production, which occurs when carbohydrate (glucose) supply is limited during NEB, can result in ketosis (Drackley et al., 2001).Metabolic adaptations in carbohydrate and protein metabolism also occur around calving (Drackley et al., 2001, 2005). Low insulin concentrations result in decreased oxidative use of glucose by peripheral tissues, thereby sparing glucose for milk synthesis. In the liver, the efficiency of gluconeogenesis from propionate increases after parturition. Glucose synthesis from glycerol and glucogenic amino acids such as alanine increases around parturition to meet the glucose demand that cannot be supplied by propionate due to low DMI. Body protein mobilization increases during the first 3 weeks postpartum to supply amino acids for both milk protein synthesis and glucose synthesis. In practical terms, this emphasizes the importance of dietary provision of metabolizable protein. Lack of response in milk production to increased rumen-undegradable protein supplementation, except in first-calf heifers (Van Saun et al., 1993; Santos et al., 2001), has been common in the literature (see Bell et al., 2000) and in our own experience (Underwood et al., 2001). Nevertheless, the importance of maintenance of maternal stores of protein on long-term health, productivity, and reproduction is backed by strong indirect evidence (Bell et al., 2000).The onset of milk synthesis creates a large drain on the blood pool of free calcium, resulting in sometimes-marked decreases in blood calcium concentration. Hypocalcemia can be classified as subclinical (blood Ca between 8 and 5.5 mg/dL) or clinical. While the incidence of clinical hypocalcemia or milk fever is low, subclinical hypocalcemia is much more prevalent and insidious. Subclinical hypocalcemia is associated with decreased smooth muscle function, which manifests as decreased motility of the rumen and abomasum (which increases risk of displaced abomasum) and decreased contraction of the teat sphincter, thus increasing risk of mastitis (Goff, 2006). Decreased feed intake (thus increasing risk of subclinical ketosis) and decreased immune cell function also result from hypocalcemia (Kimura et al., 2006). Because of these widespread effects of hypocalcemia and the decrease in smooth muscle function in the uterus, reproductive performance may be impaired.Hypocalcemia is usually assessed by sampling blood during the first 24 hours after calving, when blood Ca is at its nadir. Hypocalcemia can persist during the first several days postpartum, which can contribute to sluggish starts to lactation and increased incidence of secondary health problems such as ketosis and fatty liver. Until the ability of the digestive tract to absorb calcium can increase, calcium must be obtained by breaking down bone. Metabolic acidosis caused by a negative dietary cation-anion difference (DCAD) favors mobilization of calcium from bone, whereas high dietary potassium concentrations and positive DCAD suppress this process (Horst et al., 1997).Metabolic adaptations are directed by endocrine and central nervous system controls that to some (as yet unknown) extent monitor and respond to the degree of NEB (Drackley et al., 2001, 2005). Major endocrine changes include increased secretion of somatotropin, decreased insulin and insulin-like growth factor-1 (IGF-1), and increased glucagon. Lipolysis in adipose tissue is stimulated mainly by the sympathetic nervous system in the presence of low insulin concentrations. The sympathetic nervous system responds to energy shortage or chronic stressors with greater activity. Although stressors and severe limitations in DMI can lead to NEB before calving, the degree is much less than the severe NEB that can occur following parturition. Severe or prolonged NEB can lead to increased TAG deposition in liver, increasedketone bodies such as BHBA and acetoacetate in blood, and depletion of body reserves of energy (largely fat) and protein.Function of the immune system also is depressed during the transition period (Mallard et al., 1998). The degree of immunosuppression seems to be greater in overconditioned cows (Lacetera et al., 2005) and in cows with fatty liver (Bobe et al., 2004). Decreased ability of the immune system to respond to infectious challenges likely is responsible for the high incidence of environmental mastitis around calving, as well as the high incidence of metritis. Reasons for the decreased immune function are not well understood. Vitamins A and E as well as a number of the trace minerals (selenium, copper, zinc) play a role in enhancing immune function. Recent evidence suggests that NEB or negative protein balance may be a major contributing factor (Goff, 1999). This finding relates well to the common observation that cows which seem to be the most stressed by nutrition and environmental factors, as judged by excessive loss of body condition, are the most likely to become ill. In particular, an inadequate supply of metabolizable protein has been related to impaired function of the immune system (Houdijk et al., 2001). Recent evidence linking retained placenta to a malfunction of the immune system (Kimura et al., 2002) suggests that protein nutrition also might impact the incidence of retained placenta.Fatty liverFatty liver is defined as an accumulation of TG (the same kind of fat as found in adipose tissue, milk fat, or vegetable oils) in the liver. Fatty liver does not occur when cows are in positive energy balance and gaining weight because the liver is not a place of storage for fat like the adipose or fat tissues throughout the body (backfat, organ fat, etc.). Dietary fats provided from oilseeds such as canola or soybeans, animal fats, or commercial fat supplements are handled by the cow differently than NEFA and largely bypass the liver. In situations where milk fat is depressed by feeding excessive supplemental fats and oils perhaps with monensin, the decreased milk fat results mainly from inhibition of fatty acid synthesis in the udder by CLA and other trans-fatty acids produced in the rumen. Therefore, there should be little concern about dietary fats or milk fat-depressing diets leading to fatty liver development.While the technical name is “hepatic lipidosis”, it is also called “fatty liver syndrome”, “fat cow syndrome”, or “lipomobilization syndrome”. The term “fatty liver syndrome” is probably the best name because it indicates that many other organ systems are affected besides the liver. Fatty liver is caused by excessive uptake of nonesterified fatty acids (NEFA) mobilized from body fat (adipose tissues) in response to NEB. All cows go through some degree of NEB after calving, and essentially all cows have body fat to mobilize. Thus, all cows are at risk for developing fatty livers, even those in thin body condition. However, overconditioning certainly is a major risk factor for development of fatty livers, because fat cows do not eat as well as thinner cows and easily break down body fat to NEFA.Fatty liver usually develops after calving, with peak incidence at about 10 days in milk (Figure 1). One research study from Michigan State University found that cows which developed severe fatty livers after calving actually had significant fat accumulation in the liver during the last 3 wk before calving. However, no other studies have confirmed this pre-calving fatty liver. Fatty liver can develop quickly after calving. Estimates of rates of body fatbreakdown and liver conversion of NEFA to triglyceride indicate that a severe fatty liver could develop within one to two days after calving (Drackley et al., 2001).Unfortunately, there are no reliable methods for diagnosis of fatty liver except for liver biopsy. Ultrasound techniques are being developed but are not yet reliable. Determination of liver TG content by small-needle biopsy is a useful and accurate indicator of the degree of metabolic disturbance faced by individual cows (Jorritsma et al., 2001). Biopsies obtained between 8 and 14 days postpartum are most useful in classifying cows. Liver lipid content can be estimated microscopically as the volume of hepatocytes occupied by lipid or chemically as the concentration of TG (Table 2). Concentrations of TG <5.0% and 5.0 to <10.0% are classified as mild and moderate fatty liver, respectively, whereas severe fatty liver is considered to be >10.0% TG (Gaal et al., 1983). Severe fatty liver likely is the only form that is clinically relevant (Gerloff et al., 1986), although moderate fatty liver is also associated with greater incidences of disease and impaired reproduction (Rukkwamsuk et al., 1999; Jorritsma et al., 2000). Surveys indicate that between 25% and 65% of cows have moderate or severe fatty liver in the first weeks after calving (Bobe et al., 2004). Measurement of glycogen in liver in addition to TG increases the usefulness of the information, as concentrations of TG and glycogen vary inversely during the early postpartum period (Figure 1; Drackley et al., 2005). However, liver biopsy is an invasive and time-consuming process, and analytical determination of TAG and glycogen is not well-adapted to rapid testing.Table 2. Classification of fatty liver by concentration of triglyceride(TG) or by cell volume occupied by lipidCategory TG (% wet liver) Proportion of volume as lipidNormal healthy <1.0 <0.05Mild fatty liver 1.0 – 5.0 0.05 - 0.20Moderate fatty liver 5.0 – 10.0 0.20 - 0.40Severe fatty liver >10.0 >0.40Maintaining optimal liver function is central to the ability of cows to make a smooth transition into heavy milk production. As the degree of fatty infiltration increases, normal functions of the liver are affected adversely. Cows with fatty liver have a greater degree of immune suppression around calving (Bobe et al., 2004), which may make them more susceptible to developing infectious diseases such as mastitis and metritis. Severe fatty liver usually appears as part of a multi-factor disease complex. Fat infiltration impairs the ability of the liver to detoxify ammonia to urea (Strang et al., 1998). Ammonia decreases the ability of the liver to convert propionate to glucose (Overton et al., 1999), thus linking fat accumulation to impaired gluconeogenesis in liver (Drackley et al., 2001).Fatty liver also impairs the ability of the liver to detoxify endotoxin, and thereby renders the cow extremely sensitive to endotoxic shock and death (Andersen et al., 1996). In severe fatty liver, normal functions of the liver are severely depressed, which results in the condition of "fatty liver syndrome" or "clinical fatty liver" (Morrow, 1976). Feed intake and carbohydrate status ofthe cow are important in determining the extent of body fat mobilization, fatty liver, and ketone body production in the liver. Fat infiltration per se evidently does not lead to liver failure (Rehage, 1996) but may be a contributing factor at least in some circumstances.Figure 1. Concentrations of total lipid, triacylglycerol (triglyceride), and glycogen in liver during the periparturient period. (From Drackley et al., 2005)Fatty liver is negatively associated with fertility (Rukkwamsuk et al., 1999). This association may be an indirect effect of the extreme NEB that exists in these cows. However, there also may be direct negative effects of hepatic lipid infiltration on reproduction. Blood flow through the liver may be altered by fat accumulation expanding cell volume and compressing hepatic sinusoids. Alternately, lipid accumulation may decrease the ability of the liver to metabolize or clear reproductive hormones, thus altering the normal signaling to reproductive tissues and the pituitary.While effects of fatty liver per se on milk production are less clear, overall the evidence for impairment of dairy cow health and productivity is strong.KetosisOriginal research summarized by Kronfeld (1982) resulted in his classification of ketosis in dairy cows into four types: 1) primary underfeeding ketosis – results because “the cow is not offered enough acceptable feed,” 2) secondary underfeeding ketosis – results because “the cow’svoluntary feed intake is diminished by disease,” 3) alimentary or ketogenic ketosis – results because “the cow is consuming excessive amount of highly ketogenic feed,” and 4) spontaneous ketosis – results under a condition when the diet appears nutritionally adequate. More recently, reference to type I and type II ketosis has been made (Holtenius and Holtenius, 1996), which appears to be a much more functional differentiation in modern dairy production (Herdt, 2000a). Type I ketosis, also known as spontaneous ketosis, occurs when the demand for glucose is greater than the liver capacity for gluconeogenesis (Herdt, 2000a). This occurs when the supply of glucose precursors is limiting for maximal glucose production when the gluconeogenic pathways are at maximal capacity (Herdt, 2000a). During type I ketosis, concentrations of glucose and insulin in blood typically are low, the insulin to glucagon ratio low, concentrations of blood ketones are elevated, a high rate of mitochondrial uptake of NEFA exists, and severe fatty liver is absent (Herdt, 2000a).Fatty liver is characteristically associated with so-called “type II ketosis”. Type II ketosis occurs when large amounts of NEFA are delivered to the liver when gluconeogenesis and ketogenesis are not maximally stimulated (Herdt, 2000a). Holtenius and Holtenius (1996) suggest that type II ketosis is associated with hyperglycemia, hyperinsulinemia prior to clinical signs, insulin resistance, lower concentrations of ketone bodies in blood, and higher concentrations of glucose in blood than in type I ketosis. This is the type of ketosis that that results from overfeeding during the dry period and having overconditioned cows that are set up for liver function impairment due to their high depression of DMI around calving. Ketogenic grass silages that contain large amounts of butyric acid may be a contributing factor to fatty liver development as well as butyric acid (alimentary) ketosis.The reported prevalence of ketosis varies among farms worldwide. Over the last 10 years, ketosis (particularly type II) has become the number one reason for farm consultations by the University of Wisconsin clinical veterinary staff (G. Oetzel and K. Nordlund, personal communication, 2007). Duffield (2000) reported that subclinical ketosis prevalence worldwide varied from 8.9% to 34% for cows during the first two months of lactation. Clinical ketosis prevalence was lower and varied from 2% to 15%. Both subclinical and clinical ketosis result in economic losses for dairy producers due to decreased milk yield and poorer reproductive performance. Cows with clinical ketosis had a loss of milk of 2.5 to 3.5 kg/d in the month following diagnosis, 0.3 to 0.7 kg/d during the following month, and no long-term loss of milk (Fourichon et al., 1999). Cows with clinical ketosis had more days to first service, a lower conception rate, and increased days open (Fourichon et al., 2000).Primary ketosis can be either subclinical or clinical (Baird, 1982). Clinical signs include decreased appetite, decreased milk production, loss of BW, hypoglycemia, and hyperketonemia. Ketone bodies (BHBA and acetoacetate) are found in blood, milk, and urine. Subclinical ketosis is diagnosed at serum BHBA concentrations above 10.4 mg/dL (1000 µmol/L) and clinical ketosis is diagnosed at BHBA concentrations above 27 mg/dL (2600 µmol/L; Duffield, 2000). Duffield (2000) pointed out that the values used to set the threshold for subclinical ketosis are arbitrary and that clinical signs of ketosis can occur with a large range of serum BHBA concentrations.Triggers for Clinical DiseaseAn age-old question and problem in the study of ketosis and fatty liver is why some cows eventually go on to develop signs and clinical pathology whereas others do not, despite roughly similar clinical biochemistry values (i.e., serum NEFA and BHBA concentrations, etc.). One of the most exciting recent areas of research is the study of gene expression in liver, using “microarray” techniques. These procedures allow quantification of the mRNA expression of thousands of gene sequences simultaneously on a microscope slide-sized glass plate. We have conducted several studies that have provided new insights into the molecular mechanisms of ketosis and fatty liver development, as well as the potential triggers for clinical disease (Loor et al., 2005, 2006, 2007).Briefly, we have uncovered evidence for several potential disease-causing mechanisms in cows subjected to a feed restriction protocol to induce ketosis in early lactation (Dann et al., 2005; Loor et al., 2007). These cows had elevated BHBA concentrations in blood and increased TG in liver, typical of ketosis. The theme areas for which evidence was obtained for impaired liver cellular functions included: 1) down-regulation of genes responsive to oxidative stress (e.g., SOD1, ATOX1, PRDS2, GLRX, GSTA4, et al.), but increase of potential sources of oxidants (e.g., ACOX1, UCP1); 2) up-regulation of genes indicating enhanced DNA fragmentation and apoptosis; 3) blunted repair response to DNA damage; 4) down-regulation of components of oxidative phosphorylation, suggesting that the liver’s ability to generate ATP for its functions eventually may be impaired; 5) down-regulation of enzymes in cholesterol synthesis (e.g., HMGCR), which may impair VLDL export and contribute to greater TG accumulation; 6) down-regulation of growth hormone signaling mechanism (e.g., GHR, IFG1, SOCS2), which may disrupt normal homeostatic and homeorhetic controls; 7) down-regulation of ubiquinone synthesis and ubiquitination activity, which are involved in targeting damaged or aberrant proteins for degradation; and 8) down-regulation of components of the immune system.Our working hypothesis in this line of investigation, then, is that as the pathophysiology of NEB continues and worsens, clinical disease eventually is triggered when accumulative cell damage in liver and other tissues prevents maintenance of homeostasis. Key functions that are compromised may include mitochondrial energy status, accumulation of aberrant proteins that cannot be properly cleared, and induction of apoptosis (programmed cell death).Risk Factors for Fatty Liver and KetosisSeveral factors increase the likelihood of cows developing fatty livers and ketosis. Among these may be individual herd-specific factors, parity, body condition score, genetics, and season (Duffield, 2000; Bobe et al., 2004). As mentioned earlier, overconditiong is a clear risk factor. Cows with long calving intervals or long dry periods thus may be at greater risk. Even cows that are not overconditioned but are fed diets too rich in energy for long periods in the dry period are at greater risk to develop fatty livers after calving than are cows fed to meet their requirements during the dry period.An interesting risk factor identified in recent studies is that DMI and feeding behavior during the last 2 weeks before calving are highly predictive of health problems in individual。
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奶牛酮病研究进展
王峰;冯忠义;高慧;王林
【期刊名称】《中国畜牧兽医》
【年(卷),期】2006(33)7
【摘要】奶牛酮病是高产奶牛常见的一种营养代谢性疾病,随着奶牛生产水平的提高,其发病率也呈上升趋势.作者对奶牛酮病的病因、发病机理和临床症状进行了详细叙述,全面总结了该病的研究现状;并针对其发病机理制定了合理的防治措施,为生产上减少经济损失提供一定的理论指导.
【总页数】3页(P29-31)
【作者】王峰;冯忠义;高慧;王林
【作者单位】山东省泰安市畜牧办公室,泰安,271000;山东泰山职业技术学院,泰安,271000;山东省泰安市畜牧办公室,泰安,271000;山东农业大学动物科技学院,泰安,271000
【正文语种】中文
【中图分类】S858.23
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