Nutritional management of dairy cows to enhance gut functions

拟议研究的目的是评估新的营养管理方法，以增强肠道功能。在NSERC发现基金的支持下，我一直致力于减轻奶牛的亚急性瘤胃酸中毒（SARA）。SARA是一种代谢紊乱，对反刍动物的健康和生产力产生负面影响。饲喂高粒饲粮往往会引起过度发酵，导致发酵酸在瘤胃（反刍动物的第一个胃）中积累，导致全身炎症、采食量减少、肝脓肿、跛行等代谢紊乱。然而，值得注意的是，有些动物即使在较低的瘤胃pH值（即SARA）下也能保持较高的采食量和产奶量。观察到的动物对这种情况的不同耐受性尚不清楚，潜在的因素值得调查。对于目前的建议，我假设胰高血糖素样肽2 (GLP-2)，一种从远端肠释放的激素，在增强肠道功能和减轻SARA的负面后果中起重要作用。由于瘤胃酸中毒和过量的后肠发酵通常会增加脂多糖（一种内毒素）进入血液循环，因此增强肠道屏障功能对于减少肠道过度发酵的负面后果非常重要。众所周知，GLP-2在肠道发育和健全肠道功能中起着重要作用，但尚不清楚它如何参与最小化与SARA相关的问题。我计划使用酸中毒挑战模型，在2天50%的饲料限制后喂养5公斤磨碎的谷物，以确定是否会通过持续给药GLP-2类似物来减少SARA的负面影响。此外，我将评估几种可能提高血浆GLP-2浓度的营养管理方法，如补充丁酸盐。我推测，增强GLP-2的分泌可以减少急性期蛋白血清浓度所显示的全系统炎症。拟议的研究还将调查补充锌对肠道完整性的作用，并评估它是否能减少SARA引起的全身炎症。拟议的研究预计将通过最大限度地减少SARA引起的全身代谢问题，为加拿大的可持续乳制品生产做出贡献。

The objective of the proposed research is to evaluate novel nutritional management approaches to enhance gut functions. I have been working to mitigate sub-acute rumen acidosis (SARA) in dairy cows with the support of my NSERC Discovery Grant. The SARA is a metabolic disorder that negatively affects the health and productivity of ruminants. Feeding high grain diets often causes excess fermentation that results in the accumulation of fermentation acids in the rumen (the first stomach of ruminants), leading to systemic inflammation, feed intake reduction, liver abscesses, lameness, and other metabolic disorders. However, it is noteworthy that some animals maintain high feed intake and milk production even with low rumen pH (i.e., SARA). The variable tolerance observed among animals to this condition is not well understood, and the underlying factors warrant investigation. For the current proposal, I hypothesize that glucagon-like peptide 2 (GLP-2), a hormone released from the distal intestine, plays an important role in enhancing gut functions and mitigates the negative consequences of SARA. Because rumen acidosis and excess hind-gut fermentation often increases the entry of lipopolysaccharide, an endotoxin, into blood circulation, enhancing gut barrier function is considered very important to minimize the negative consequences of excess fermentation in the gut. It is well established that GLP-2 plays an important role in gut development and sound gut function, but it is not known how it is involved in minimizing problems related to SARA. I plan to use an acidosis challenge model, where 5 kg of ground grain will be fed after a 2-d 50% feed restriction, to determine if negative effects of SARA would be reduced by continuous administration of a GLP-2 analogue. Furthermore, I will evaluate several nutritional management approaches to potentially enhance plasma GLP-2 concentration, such as butyrate supplementation. I hypothesize that enhancing GLP-2 secretion will minimize systemic inflammation indicated by the serum concentration of acute phase proteins. The proposed research will also investigate the role of supplemental zinc on gut integrity and evaluate if it would minimize systemic inflammation caused by SARA. The proposed research is expected to contribute to sustainable dairy production in Canada by minimizing systemic metabolic problems caused by SARA.