Systems Biology and Ruminal Acidosis
Dairy cattle are commonly transitioned to a diet that is rich in rapidly fermentable carbohydrates (high-grain) to increase milk production in early lactation. When the shift in diet is too abrupt or the grain level too high, the rate of ruminal fermentat
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Systems Biology and Ruminal Acidosis Morteza H. Ghaffari, Ehsan Khafipour, and Michael A. Steele
Abstract
Dairy cattle are commonly transitioned to a diet that is rich in rapidly fermentable carbohydrates (high-grain) to increase milk production in early lactation. When the shift in diet is too abrupt or the grain level too high, the rate of ruminal fermentation exceeds the rate of ruminal absorption and buffering, making the cow susceptible to ruminal acidosis. Most investigations of ruminal acidosis have taken a reductionist approach and focused on the impact on the rumen without considering other organs. However, the impact of grain-induced ruminal acidosis involves a whole animal inflammatory response and it is becoming increasingly evident that other gut compartments, namely the lower gut and visceral tissue such as the liver, also play an important role in the etiology of whole animal, multi-organ inflammatory response. Over the past decade, characterizing the gastrointestinal tract and whole animal inflammatory response to grain- induced ruminal acidosis has been initiated using a systems biology approach. To accomplish this, combinations of high-throughput omics-data (i.e., genomics, metabolomics, transcriptomics, and proteomics) have produced unique and meaningful advances in our understanding of the etiology of ruminal acidosis. This chapter will focus on the application of systems biology relating to ruminal acidosis, which provides meaningful insight into the ruminal microbial ecology, metabolome, and host gene expression changes during ruminal acidosis.
M.H. Ghaffari • M.A. Steele, Ph.D. (*) Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, AB, Canada e-mail: [email protected]; [email protected] E. Khafipour, Ph.D. Departments of Animal Science and Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada e-mail: [email protected] © Springer International Publishing Switzerland 2017 B.N. Ametaj (ed.), Periparturient Diseases of Dairy Cows, DOI 10.1007/978-3-319-43033-1_4
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M.H. Ghaffari et al.
Introduction
Intensive dairy production systems rely on large amounts of grain in diets to increase energy intake to support high levels of milk production. However, feeding excessive amounts of rapidly fermentable dietary carbohydrate to ruminants causes a shift in the rumen microbiota which leads to an accumulation of short-chain fatty acids (SCFA) and a depression of ruminal pH. These changes lead to the digestive disorder termed ruminal acidosis (Khafipour et al. 2009a). When ruminal pH drops to 5.6 or below, the microbial populations in the rumen shift toward the production of lactic acid, which further decreases rumen pH. Lactic acid has a much lower pKa compared to volatile fatty acids (pKa 3.9 vs.4.9) and it is less protonated compared to SCFA at pH 5.0. As a result, lactic acid accumulates in the rumen and leads to a downward spiral in ruminal pH (Nagaraja and Titgemeyer 2007). The subacute form of ruminal acidosis (S
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