Milk protein yield responses to changes in the profile of essential amino acids absorbed by the gastrointestinal tract or circulating in blood plasma do not follow the classic limiting amino acid response, in part because of an ability of the mammary glands to modify their blood flow rate and net clearance of amino acids out of plasma. The hypothesis that mammary blood flow is locally regulated to maintain ATP balance accounts for observed changes in flow due to postruminal glucose, insulin, and essential amino acid (EAA) infusions. An additional hypothesis that net mammary uptakes of metabolites from blood are affected by perturbations in their respective arterial concentrations and the rate of mammary blood flow also appears to hold for the energy metabolites glucose, acetate, β-hydroxybutyrate, and fatty acids. However, net EAA uptakes by the mammary glands are poorly predicted by models considering arterial concentrations and blood flow rates only. Evidence points to intramammary protein synthesis and secretion as the determinant of net EAA uptake. The intracellular signaling network anchored by the mechanistic target of rapamycin complex 1 stands as an excellent candidate to explain nutritional effects on milk protein synthesis because it integrates information on physiological and nutritional state to affect protein synthesis and cell metabolism, growth, proliferation, and differentiation in many cell types. In mammary cells in vitro and in vivo, the mechanistic target of rapamycin complex 1, integrated stress response, and glycogen synthase kinase-3 networks that contribute to regulation of initiation of mRNA translation are responsive to acute changes in nutrient supply and EAA profile. However, after several days of postruminal infusion of balanced and imbalanced EAA profiles, these signaling networks do not appear to continue to account for changes in milk protein yields. Gene expression evidence suggests that regulation of components of the unfolded protein response that control biogenesis of the endoplasmic reticulum and differentiation of a secretory phenotype may contribute to effects of nutrition on milk protein yield. Connections between early signaling events and their long-term consequences should be sought.

牛奶蛋白对胃肠道吸收或血浆中循环的必需氨基酸谱变化的响应不遵循经典的限制性氨基酸响应，部分原因是乳腺有能力改变其血流速度和血浆中氨基酸的净清除率。乳腺血流被局部调节以维持ATP平衡的假说解释了由于瘤胃后葡萄糖，胰岛素和必需氨基酸（EAA）输注而引起的血流变化。另一个假设是，血液中代谢物的净乳腺摄取受其各自动脉浓度的扰动影响，并且乳血流的速率对于能量代谢物葡萄糖，乙酸盐，β-羟基丁酸酯和脂肪酸也成立。然而，仅考虑动脉浓度和血流速度的模型很难预测乳腺的净EAA摄入量。有证据表明，乳内蛋白质的合成和分泌是EAA净摄入量的决定因素。雷帕霉素复合物1的机械靶标锚定的细胞内信号网络是解释对牛奶蛋白质合成的营养作用的极佳候选者，因为它整合了有关生理和营养状态的信息，从而影响蛋白质合成和细胞代谢，生长，增殖和分化。许多细胞类型。在体外和体内的乳腺细胞中，雷帕霉素复合物1的机制靶标整合了应激反应，有助于调节mRNA翻译起始的糖原合酶激酶3网络对营养供应和EAA分布的急性变化有反应。然而，在瘤胃中注入平衡和不平衡的EAA谱图几天后，这些信号网络似乎无法继续解释乳蛋白产量的变化。基因表达证据表明，调控内质网生物发生和分泌表型分化的未折叠蛋白质反应成分的调节可能有助于营养对牛奶蛋白质产量的影响。应寻求早期信号事件与其长期后果之间的联系。这些信号网络似乎无法继续解释乳蛋白产量的变化。基因表达证据表明，调控内质网生物发生和分泌表型分化的未折叠蛋白质反应成分的调节可能有助于营养对牛奶蛋白质产量的影响。应寻求早期信号事件与其长期后果之间的联系。这些信号网络似乎并不能继续解释乳蛋白产量的变化。基因表达证据表明，调控内质网生物发生和分泌表型分化的未折叠蛋白质反应成分的调节可能有助于营养对牛奶蛋白质产量的影响。应寻求早期信号事件与其长期后果之间的联系。