Rouvinen-Watt Kirsti
Nova Scotia Agricultural College, Department of Plant and Animal Sciences, P.O. Box 550, Truro, Nova Scotia B2N 5E3.
Can J Vet Res. 2003 Jul;67(3):161-8.
Nursing sickness, the largest single cause of mortality in adult female mink (Mustela vison), is an example of a metabolic disorder, which develops when the demands for lactation require extensive mobilization of body energy reserves. The condition is characterized by progressive weight loss, emaciation, and dehydration with high concentrations of glucose and insulin in the blood. Morbidity due to nursing sickness can be as high as 15% with mortality around 8%, but the incidence is known to vary from year to year. Stress has been shown to trigger the onset of the disease and old females and females with large litters are most often affected. Increasing demand for gluconeogenesis from amino acids due to heavy milk production may be a predisposing factor. Glucose metabolism is inextricably linked to that of protein and fats. In obesity (or lipodystrophy), the ability of adipose tissue to buffer the daily influx of nutrients is overwhelmed (or absent), interfering with insulin-mediated glucose disposal and leading to insulin resistance. Polyunsaturated fatty acids of the n-3 family play an important role in modulating insulin signalling and glucose uptake by peripheral tissue. The increasing demand on these fatty acids for milk fat synthesis towards late lactation may result in deficiency in the lactating female, thus impairing glucose disposal. It is suggested that the underlying cause of mink nursing sickness is the development of acquired insulin resistance with 3 contributing key elements: obesity (or lipodystrophy), n-3 fatty acid deficiency, and high protein oxidation rate. It is recommended that mink breeder females be kept in moderate body condition during fall and winter to avoid fattening or emaciation. A dietary n-3 fatty acid supplement during the lactation period may be beneficial for improved glycemic control. Lowering of dietary protein reduces (oxidative) stress and improves water balance in the nursing females and may, therefore, prevent the development and help in the management of nursing sickness. It is also surmised that other, thus far unexplained, metabolic disorders seen in male and female mink may be related to acquired insulin resistance.
母貂泌乳期疾病是成年雌性水貂(鼬属)死亡的最大单一原因,是一种代谢紊乱的例子,当泌乳需求需要大量调动身体能量储备时就会出现这种情况。这种病症的特征是体重逐渐减轻、消瘦和脱水,同时血液中葡萄糖和胰岛素浓度很高。母貂泌乳期疾病的发病率可能高达15%,死亡率约为8%,但已知发病率每年都有所不同。已证明压力会引发该病,老龄母貂和产仔多的母貂最常受到影响。由于大量产奶导致对氨基酸糖异生的需求增加可能是一个诱发因素。葡萄糖代谢与蛋白质和脂肪的代谢有着千丝万缕的联系。在肥胖(或脂肪营养不良)状态下,脂肪组织缓冲每日营养物质流入的能力不堪重负(或缺乏),干扰胰岛素介导的葡萄糖处理,导致胰岛素抵抗。n-3族多不饱和脂肪酸在调节胰岛素信号传导和外周组织对葡萄糖的摄取方面发挥着重要作用。在泌乳后期,对这些脂肪酸用于乳脂肪合成的需求增加,可能导致泌乳母貂缺乏这些脂肪酸,从而损害葡萄糖处理。有人认为,水貂母貂泌乳期疾病的根本原因是获得性胰岛素抵抗的发展,有三个关键因素:肥胖(或脂肪营养不良)、n-3脂肪酸缺乏和高蛋白氧化率。建议在秋冬季节将母貂饲养在中等身体状况下以避免肥胖或消瘦。在泌乳期补充膳食n-3脂肪酸可能有利于改善血糖控制。降低日粮蛋白质水平可减轻(氧化)应激,改善泌乳母貂的水平衡状况,因此可能预防该病的发生并有助于该病的管理。也有人推测,在雄性和雌性水貂中出现的其他目前无法解释的代谢紊乱可能与获得性胰岛素抵抗有关。