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      Urinary Metabolomics around Parturition Identifies Metabolite Alterations in Dairy Cows Affected Postpartum by Lameness: Preliminary Study

      , , , , ,
      Dairy
      MDPI AG

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          Abstract

          (1) Background: The objective of this study was to evaluate the urine of dairy cows for presence of metabolites with the potential to be used as screening biomarkers for lameness as well as to characterize pre-lame, lame, and post-lame cows from the metabolic prospective. (2) Methods: Six lame and 20 control healthy cows were used in this nested case-control study. Urinary 1H-NMR analysis was used to identify and measure metabolites at five time points including −8 and −4 weeks prepartum, lameness diagnosis week (1–3 weeks postpartum) as well as at +4 and +8 weeks after calving. (3) Results: A total of 90 metabolites were identified and measured in the urine. At −8 and −4 weeks, 27 prepartum metabolites were identified as altered, at both timepoints, with 19 and 5 metabolites excreted at a lower concentration, respectively. Additionally, a total of 8 and 22 metabolites were found at greater concentration in pre-lame cows at −8 and −4 weeks, respectively. Lame cows were identified to excrete, at lower concentrations, seven metabolites during a lameness event with the top five most important metabolites being Tyr, adipate, glycerate, 3-hydroxy-3-methylglutarate, and uracil. Alterations in urinary metabolites also were present at +4 and +8 weeks after calving with N-acetylaspartate, glutamine, imidazole, pantothenate, beta-alanine and trimethylamine, with the greatest VIP (variable importance in projection) score at +4 weeks; and hipurate, pantothenate 1,3-dihydroxyacetone, galactose, and Tyr, with the greatest VIP score at +8 weeks postpartum. (4) Conclusions: Overall, results showed that urine metabotyping can be used to identify cows at risk of lameness and to better characterize lameness from the metabolic prospective. However, caution should be taken in interpretation of the data presented because of the low number of replicates.

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          Liver regulation of acid-base balance.

          Traditionally, lungs and kidneys have been viewed as the sole and principal organs involved in systemic acid-base homeostasis in mammals, but this view is not entirely compatible with basic principles of chemistry. Recent conceptual developments point to a role for the liver in pH homeostasis in addition to the well-established role of lungs and kidneys. Hepatic and renal nitrogen metabolism are linked by an interorgan glutamine flux, which couples both renal ammoniagenesis and hepatic ureogenesis to systemic acid-base regulation. Hepatic urea synthesis is a major pathway for the removal of metabolically generated bicarbonate. A structural-functional organization in the liver acinus uncouples urea cycle flux control from the vital need to maintain ammonium homeostasis. There is a sensitive and complex control of bicarbonate disposal via hepatic ureogenesis by the extracellular acid-base status, suggestive of a feedback control loop between acid-base status and the rate of bicarbonate elimination, i.e., a hepatic bicarbonate-homeostatic response. Some pathophysiological implications arising from the pH-stat function of the liver are discussed.
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            The role of liver in acid-base regulation

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              Glucose and short-chain fatty acid metabolism

              Brockman (1993)
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                Author and article information

                Contributors
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                Journal
                Dairy
                Dairy
                MDPI AG
                2624-862X
                December 2020
                March 13 2020
                : 1
                : 1
                : 2
                Article
                10.3390/dairy1010002
                86f70c7a-fc90-42e6-ac9c-2fd024ddefea
                © 2020

                https://creativecommons.org/licenses/by/4.0/

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