Global warming and accompanying high ambient temperatures reduce feed intake of dairy cows and shift the blood flow from the core of the body to the periphery. As a result, hypoxia may occur in the digestive tract accompanied by disruption of the intestinal barrier, local endotoxemia and inflammation, and altered nutrient absorption. However, whether the barrier of the rumen, like the intestine, is affected by ambient heat has not been studied so far. Lactating Holstein dairy cows were subjected to heat stress at 28°C (temperature-humidity index = 76; n = 5) with ad libitum feed intake or to thermoneutral conditions at 15°C (temperature-humidity index = 60; n = 5) and pair-feeding to heat-stressed animals for a total of 4 d. Gas exchange and feed intake behavior were measured in a respiration chamber, and rumen epithelia were taken after slaughter. Heat stress significantly reduced meal size and whole-body fat oxidation but increased meal frequency and carbohydrate oxidation. The mRNA expression of toll-like receptor 4 (TLR4) and tight junction proteins and the phosphorylation of TLR4 downstream targets (interleukin-1 receptor-associated kinase 4, stress-activated protein kinase, p38 mitogen-activated protein kinase, and nuclear factor k-B) in the rumen epithelium were not affected by heat. The proteomics approach revealed increased expression of rumen epithelium proteins involved in the AMP-activated protein kinase (AMPK) and insulin signaling pathways in heat-stressed cows. Also, proteins involved in chaperone-mediated folding of proteins were upregulated, whereas those involved in antioxidant defense system were downregulated. Further, we found evidence for increased carbohydrate phosphorylation accompanied with an increased flux of carbohydrates through the hexosamine biosynthetic pathway, providing substrates for protein glycosylation. In conclusion, the mild heat stress did not induce barrier dysfunction or inflammatory responses in the rumen epithelium of dairy cows, probably because of adaptations in feed intake behavior and defense mechanisms at the tissue level.

全球变暖和随之而来的高环境温度降低了奶牛的采食量，并使血流从人体核心转移到外围。结果，在消化道中可能会发生缺氧，并伴有肠屏障的破坏，局部内毒素血症和炎症以及营养吸收的改变。然而，迄今为止，尚未研究瘤胃的壁垒（如肠）是否受到环境热量的影响。哺乳的荷斯坦奶牛在自由采食的情况下于28°C（温度-湿度指数= 76; n = 5）受到热应激，或在15°C（温度-湿度指数= 60; n = 5）处于热中性条件下对热应激动物进行成对饲养，共4天。在呼吸室内测量气体交换和采食行为，宰杀后取瘤胃上皮。热应激显着减少了进餐量和全身脂肪氧化，但增加了进餐频率和碳水化合物氧化。Toll样受体4（TLR4）和瘤胃上皮中TLR4下游靶标（白介素1受体相关激酶4，应力激活蛋白激酶，p38丝裂原激活蛋白激酶和核因子kB）的紧密连接蛋白和磷酸化不受热影响。蛋白质组学方法揭示了热应激奶牛参与AMP激活的蛋白激酶（AMPK）和胰岛素信号通路的瘤胃上皮蛋白表达增加。同样，参与伴侣介导的蛋白质折叠的蛋白质被上调，而参与抗氧化剂防御系统的蛋白质被下调。此外，我们发现有证据表明，碳水化合物的磷酸化增加，同时碳水化合物通过六胺生物合成途径的流量增加，为蛋白质糖基化提供了底物。结论，