Early-lactating dairy cows mobilize body protein, primarily from skeletal muscle, to provide amino acids which are directed towards gluconeogenesis and milk protein synthesis. Propylene glycol (PG) is a precursor of ruminal propionate, and our hypothesis was that its dietary inclusion could attenuate skeletal muscle wasting by reducing amino acid-driven gluconeogenesis. The major objectives of this study were to delineate the effects of pre- and post-partum PG supplementation in transition dairy cows on whole-body nitrogen (N) balance, urinary 3-methylhistidine (3-MH) excretion, body composition, and gene expression profiles for the major protein degradation pathways in skeletal muscle. Sixteen pregnant cows (7 primiparous and 9 multiparous) were paired based on expected calving dates and then randomly assigned within each pair to either a basal diet (control) or basal diet plus 600 mL/d of PG (PG). Diets were fed twice daily for ad libitum intake, and PG was fed in equal amounts as a top dress. All measurements were conducted at 3 time intervals starting at d -14 ± 5, d 15 and d 38 relative to calving. Propylene glycol had no effect (P > 0.05) on whole-body N balance, urinary 3-MH excretion, and body composition. However, N balance was lower (P < 0.001) at d 15 and d 38, compared to d -14. Urinary excretion of 3-MH was lower at d -14 than at d 15 (P = 0.01) and d 38 (P = 0.001). Supplemental PG had no effect (P > 0.05) on body weight (BW), and all components of empty BW. On average, cows fed both diets mobilized 19 kg of body fat and 14 kg of body protein between d -14 and d 38. Supplemental PG had no effect on mRNA abundance in skeletal muscle for m-calpain (P = 0.96) and 14-kDa ubiquitin-carrier protein E2 (14-kDa E2) (P = 0.54); however, PG supplementation down-regulated mRNA expression for µ-calpain at d 15 (P = 0.02), and tended to down-regulate mRNA expression for ubiquitin at d 15 (P = 0.07) and proteasome 26S subunit-ATPase at d 38 (P = 0.097). Relative to calving, mRNA abundance for m-calpain (P = 0.02) and µ-calpain (P = 0.005) were higher at d 15 compared to d -14 and d 38. Messenger RNA abundance for ubiquitin (P = 0.07) and 14-kDa E2 (P = 0.005) were lower at d 38 compared to d 15. In summary, these results demonstrate that up-regulation of the Ca2+-dependent and ubiquitin-mediated proteolytic pathways are the mechanisms by which skeletal muscle wasting occurs in early-lactating cows. In addition, dietary supplementation with PG may down-regulate some of these proteolytic pathways, thereby potentially attenuating undesirable skeletal muscle wasting.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:SSU.etd-03132008-122513 |
Date | 18 March 2008 |
Creators | Chibisa, Gwinyai Emmanuel |
Contributors | Van Kessel, Andrew G., Mutsvangwa, Tim, Christensen, David A., Buchanan, Fiona C., Zello, Gordon A. |
Publisher | University of Saskatchewan |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | text |
Format | application/pdf |
Source | http://library.usask.ca/theses/available/etd-03132008-122513/ |
Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Saskatchewan or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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