To meet the energy requirements of high-yielding dairy cows, grains and fats have increasingly been incorporated in ruminant diets. Moreover, lipid supplements have been included in ruminant diets under experimental or practical conditions to increase the concentrations of bioactive n-3 fatty acids and conjugated linoleic acids in milk and meat. Nevertheless, those feeding practices have dramatically increased the incidence of milk fat depression in dairy cattle. Although induction of milk fat depression may be a management tool, most often, diet-induced milk fat depression is unintended and associated with a direct economic loss. In this review, we give an update on the role of fatty acids, particularly originating from rumen biohydrogenation, as well as of rumen microbes in diet-induced milk fat depression. Although this syndrome seems to be multi-etiological, the best-known causal factor remains the shift in rumen biohydrogenation pathway from the formation of mainly trans-11 intermediates toward greater accumulation of trans-10 intermediates, referred to as the trans-11 to trans-10 shift. The microbial etiology of this trans-11 to trans-10 shift is not well understood yet and it seems that unraveling the microbial mechanisms of diet-induced milk fat depression is challenging. Potential strategies to avoid diet-induced milk fat depression are supplementation with rumen stabilizers, selection toward more tolerant animals, tailored management of cows at risk, selection toward more efficient fiber-digesting cows, or feeding less concentrates and grains.

为了满足高产奶牛的能量需求，反刍动物日粮中越来越多地添加了谷物和脂肪。此外，在实验或实际条件下，反刍动物日粮中还添加了脂质补充剂，以增加牛奶和肉中生物活性n-3脂肪酸和共轭亚油酸的浓度。然而，这些喂养方式大大增加了奶牛乳脂降低的发生率。尽管诱发乳脂降低可能是一种管理工具，但大多数情况下，饮食诱导的乳脂降低是意料之外的，并直接造成经济损失。在这篇综述中，我们提供了脂肪酸的作用的最新信息，特别是源自瘤胃生物氢化作用的脂肪酸以及瘤胃微生物在饮食引起的牛奶脂肪减少中的作用。反式-11中间体向反式-10中间体的更大积累，称为反式-11向反式-10转移。从反式-11到反式-10转变的微生物病因尚未得到很好的理解，并且似乎难以弄清饮食引起的乳脂降低的微生物机制。避免饮食引起的牛奶脂肪减少的潜在策略是补充瘤胃稳定剂，选择对耐受性更高的动物，对有风险的母牛进行有针对性的管理，选择对纤维消化效率更高的母牛的选择，或饲喂较少的精矿和谷物。