Nutritional regulation of rumen epithelium

商业乳制品生产系统依赖于具有高水平的可快速发酵的碳水化合物的能量密集饮食来提高生产效率。 然而，反刍动物食用高谷物/低纤维饮食通常导致挥发性脂肪酸（VFA）和乳酸在瘤胃内积累，引起瘤胃酸中毒。 酸中毒的影响包括采食量减少、瘤胃上皮损伤，随后可导致肝损伤、蹄叶炎和死亡。本研究计划将描述酸中毒诱导模型和疾病对瘤胃上皮细胞周转和调节蛋白质周转的基因表达的影响。 这一全面的生物学模型将允许随后发展的营养策略，以提高瘤胃上皮细胞的适应和恢复瘤胃酸中毒。 核心假设是：在患有亚急性瘤胃酸中毒的泌乳奶牛中，瘤胃乳酸的减少沿着亮氨酸的治疗性处理将减少蛋白质降解途径并增加瘤胃上皮细胞的增殖。 这项研究计划将导致消化功能，生产力和泌乳奶牛的福祉的改善。

Commercial dairy production systems rely on energy dense diets with elevated levels of rapidly fermentable carbohydrates to improve production efficiency. However, consumption of high grain/low-fibre diets by ruminants commonly leads to an accumulation of volatile fatty acids (VFAs) and lactate within the rumen causing ruminal acidosis. The impacts of acidosis include reduced feed intake, rumen epithelium damage and, subsequently, can lead to liver damage, laminitis and death. This program of study will characterize an acidosis-induction model and the impacts of the disease on rumen epithelial cell turnover and expression of genes regulating protein turnover. This comprehensive biological model will allow subsequent development of nutritional strategies to enhance rumen epithelium adaptation and recovery to ruminal acidosis. The central hypothesis is; in lactating cows suffering from subacute ruminal acidosis the reduction of ruminal lactate along with therapeutic treatment with leucine will reduce protein degradation pathways and increase cell proliferation of the rumen epithelium. This program of study will lead to improvements in the digestive function, productivity and well-being of lactating dairy cows.