Skip to content
University of Maryland LibrariesDigital Repository at the University of Maryland
    • Login
    View Item 
    •   DRUM
    • Theses and Dissertations from UMD
    • UMD Theses and Dissertations
    • View Item
    •   DRUM
    • Theses and Dissertations from UMD
    • UMD Theses and Dissertations
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Denovo synthesized fatty acids as regulators of milk fat synthesis

    Thumbnail
    View/Open
    Vyas_umd_0117E_12753.pdf (3.012Mb)
    No. of downloads: 1002

    Date
    2011
    Author
    Vyas, Diwakar
    Advisor
    Erdman, Richard A
    Metadata
    Show full item record
    Abstract
    The objectives of the dissertation research were to determine the role of <italic>denovo</italic> synthesized fatty acids (DNFA) in the regulation of milk fat synthesis. Milk fat responses to increasing amounts of short- and medium-chain fatty acids (SMCFA), added in the proportion as synthesized <italic>denovo</italic>, were studied in lactating dairy cows. The results showed a significant linear increase in milk fat concentration with SMCFA supplementation. However, milk fat yield was similar for all treatments. A subsequent study was aimed at increasing the availability of SMCFA during <italic>trans</italic>-10, <italic>cis</italic>-12 CLA-induced milk fat depression (MFD) in lactating dairy cows to determine whether SMCFA can rescue part of CLA-induced MFD. Post-ruminal infusion of butterfat (BF) was used as a source of SMCFA. The BF treatment was compared to a mixture of fats containing only the long-chain FA (LCFA) with or without <italic>trans</italic>-10, <italic>cis</italic>-12 CLA infusion. Milk fat content and yield were significantly reduced with <italic>trans</italic>-10, <italic>cis</italic>-12 CLA. However, increased availability of SMCFA with BF infusion had no effects on milk fat yield and concentration. <italic>Trans</italic>-10, <italic>cis</italic>-12 CLA significantly reduced the mRNA expression of transcription factor <italic>SREBP-1c</italic> along with its downstream targets including <italic>ACC</italic>,<italic>FASN</italic>, <italic>LPL</italic>, <italic>SCD</italic> and <italic>AGPAT</italic>. The increased availability of SMCFA had no effect on either lipogenic gene or protein expression suggesting that nutritional manipulation was not sufficient to rescue <italic>trans</italic>-10, <italic>cis</italic>-12 CLA-induced MFD. Finally, the effects of combination of a Rosiglitazone (ROSI), a <italic>PPAR-&#947;</italic> agonist, and <italic>trans</italic>-10, <italic>cis</italic>-12 CLA were examined on mammary and hepatic lipogenesis in lactating mice. Mammary lipogenesis was significantly reduced with <italic>trans</italic>-10, <italic>cis</italic>-12 CLA, reducing the milk fat content and mRNA expression of lipogenic transcription factors <italic>SREBP1-c</italic> and <italic>PPAR- &#947;</italic>. <italic>Trans</italic>-10, <italic>cis</italic>-12 CLA significantly increased hepatic lipid accumulation, while the mRNA expression of <italic>SREBP1-c</italic> and <italic>PPAR- &#947;</italic> were not altered. On the contrary, ROSI had no effects on mammary lipogenesis. However, ROSI significantly rescued <italic>trans</italic>-10, <italic>cis</italic>-12 CLA-induced hepatic steatosis.
    URI
    http://hdl.handle.net/1903/12306
    Collections
    • Animal & Avian Sciences Theses and Dissertations
    • UMD Theses and Dissertations

    DRUM is brought to you by the University of Maryland Libraries
    University of Maryland, College Park, MD 20742-7011 (301)314-1328.
    Please send us your comments.
    Web Accessibility
     

     

    Browse

    All of DRUMCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects

    My Account

    LoginRegister
    Pages
    About DRUMAbout Download Statistics

    DRUM is brought to you by the University of Maryland Libraries
    University of Maryland, College Park, MD 20742-7011 (301)314-1328.
    Please send us your comments.
    Web Accessibility