Effects of hindgut buffers on intestinal fermentation and microbiota in dairy cattle
Date
2024
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Publisher
University of Delaware
Abstract
Lactation in dairy cattle is an energetically costly process, leading cows to pull resources from bodily stores if energy and nutrients are not sufficiently provided in the diet. Producers regularly feed energetically dense diets to lactating cows, typically by feeding increased levels of rapidly fermentable carbohydrates like starch. However, increased dietary starch can induce acidosis along the gastrointestinal tract, both in the rumen and hindgut. Increased starch levels may lead to rapid declines in pH due to increased volatile fatty acid (VFA) and lactate production, which can degrade the rumen and intestinal epithelial barriers. Additionally, increased starch levels and the subsequent changes to digesta pH affect the gastrointestinal microbiota, encouraging microbial dysbiosis through the death of fiber-fermenting bacteria and the release of lipopolysaccharide (LPS). LPS is highly immunogenic and induces inflammation when entering systemic circulation through disrupted epithelial barriers, negatively impacting animal well-being and milk production. Thus, dietary tools to mitigate acidosis events may positively contribute to animal health and production. ☐ Ruminal acidosis has been widely studied over the years, and the use of dietary buffers to counteract the effects of high starch diets on rumen pH is common. However, high levels of dietary starch may still increase the amount of undigested starch entering the intestines, potentially leading to hindgut acidosis regardless of apparent rumen health. The first objective of this dissertation was to assess the effects of hindgut acidosis from corn starch on the intestinal fermentation and microbiome, nutrient digestibility, and systemic inflammation. The second objective was to evaluate whether two buffers (buffer A: blend of calcium carbonate, magnesium oxide and crushed oyster shell; buffer B: magnesium oxide) could alter these factors, ideally counteracting the negative effects of hindgut acidosis. Two experiments were conducted to achieve these objectives, one in vivo and one in vitro. ☐ In vivo abomasal infusions of corn starch decreased fecal pH and dry matter and starch digestibilities, and increased lymphocyte immunometabolic signaling as compared to the control. Corn starch infusions did not increase milk production, fecal LPS and total VFA, or serum acute phase proteins, and minimally affected measures of fecal microbial diversity as compared to the control. Lack of effects on acute phase proteins and the intestinal fermentation profile and microbiome were surprising, but this was likely due to unintentional SARA induction due to the moderately high starch total mixed ration. Buffer addition increased fecal pH, increased fecal acetate and total VFA, and decreased fecal score as compared to infused starch alone. Responses of serum acute phase proteins, lymphocyte immunometabolic signaling, and the fecal microbiome depended on the type and dosage of buffer. Buffer A, particularly at a higher dosage, increased serum acute phase proteins, and exaggerated negative responses to acidosis in immunometabolic signaling and the fecal microbiome. Signals related to immune response were increased while microbial taxa associated with inflammation increased in abundance. Buffer B in turn seemed to alleviate negative responses due to acidosis, reducing immunometabolic signaling and increasing the relative abundance of beneficial microbial taxa. ☐ In vitro corn starch inclusion increased cumulative gas production, lactate, butyrate, LPS, and total protein, and decreased culture pH, propionate, and ammonia nitrogen as compared to the control. Additionally, corn starch decreased the relative abundance of fibrolytic microbes and increased the relative abundance of amylolytic bacteria. Buffer inclusion in the presence of corn starch further increased gas production, acetate, propionate, butyrate, and culture pH, but did not affect culture microbiome. In the absence of corn starch both buffers A and B increased acetate and total VFA and changed microbial beta diversity as compared to the control, but buffer B additionally increased culture pH and microbial alpha diversity, seemingly improving maintenance of microbial functionality. ☐ Overall, starch inclusion induced changes to fermentation profiles both in vivo and in vitro, but only meaningfully changed microbial profiles in vitro. Increased immunometabolic lymphocyte signaling, particularly pro-inflammatory signaling, suggests negative systemic effects due to starch infusions. In vitro decreases in pH and increases in LPS corroborate this induction of inflammation seen in the in vivo experiments, and changes in microbial beta diversity and taxa relative abundance due to starch suggest contribution to microbial dysbiosis. Buffer inclusion, both in vivo and in vitro, increased fecal pH and VFA concentration. In vivo, buffer A induced additional pro-inflammatory signaling, and at the higher dosage negatively impacted the fecal microbiome, while not affecting culture microbiome in vitro in the presence of starch. Buffer B decreased pro-inflammatory signaling in vivo and impacted the fecal microbiome, but again did not affect culture microbiome in the presence of starch when evaluated in vitro. In summary, starch inclusion induced acidotic conditions in both trials, suggesting a more pro-inflammatory and dysbiotic profile as compared to the control. Buffers increased fecal pH in the presence of starch but also increased VFA concentration. Buffer A and B differentially affected immunometabolic signaling and the fecal microbiome, with buffer B producing the more diverse microbial profile. Despite the increased pH, buffer inclusion in the presence of high starch increased VFA, potentially further challenging cows. Although buffers consistently aided in raising intestinal pH, effects on hindgut health were variable between buffer types.
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Keywords
Lactation, Volatile fatty acid, Lipopolysaccharide, Immunometabolic signaling