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New DCP support studies

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    dsade's Avatar
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    New DCP support studies


    PPARα agonists up-regulate organic cation transporters in rat liver cells
    Sebastian Luci, Stefanie Geissler, Bettina König, Alexander Koch, Gabriele I. Stangl, Frank Hirche, Klaus Eder ,


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    Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, Emil-Abderhalden-Strasse 26, D-06108 Halle (Saale), Germany

    Received 15 September 2006; Available online 27 September 2006.


    Abstract

    It has been shown that clofibrate treatment increases the carnitine concentration in the liver of rats. However, the molecular mechanism is still unknown. In this study, we observed for the first time that treatment of rats with the peroxisome proliferator activated receptor (PPAR)-α agonist clofibrate increases hepatic mRNA concentrations of organic cation transporters (OCTNs)-1 and -2 which act as transporters of carnitine into the cell. In rat hepatoma (Fao) cells, treatment with WY-14,643 also increased the mRNA concentration of OCTN-2. mRNA concentrations of enzymes involved in carnitine biosynthesis were not altered by treatment with the PPARα agonists in livers of rats and in Fao cells. We conclude that PPARα agonists increase carnitine concentrations in livers of rats and cells by an increased uptake of carnitine into the cell but not by an increased carnitine biosynthesis.





    Keywords: Carnitine; Peroxisome proliferator activated receptor α; Rat; Organic cation transporter





    PPARα Agonists Reduce 11β-Hydroxysteroid Dehydrogenase Type 1 in the Liver
    Anne Hermanowski-Vosatkaa, 1, David Gerholdb, Steven S. Mundta, Vilert A. Lovinga, Meiqing Lub, Yuli Chenc, Alex Elbrechtc, Margaret Wuc, Thomas Doebberc, Linda Kellyc, Denise Milota, Qiu Guoa, Pei-Ran Wanga, Marc Ippolitoa, Yu-Sheng Chaoa, Samuel D. Wrighta, Rolf Thieringera


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    a Department of Atherosclerosis and Endocrinology, Merck Research Laboratories, 126 East Lincoln Avenue, Rahway, New Jersey

    c Department of Molecular Endocrinology, Merck Research Laboratories, 126 East Lincoln Avenue, Rahway, New Jersey

    b Department of Genomic Pharmacology, Merck Research Laboratories, 126 East Lincoln Avenue, Rahway, New Jersey

    Received 8 November 2000; Available online 27 March 2002.


    Abstract

    11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) is an enzyme that converts cortisone to the active glucocorticoid, cortisol. Cortisol–cortisone interconversion plays a key role in the regulation of glucose metabolism, since mice deficient in 11βHSD1 are resistant to diet-induced hyperglycemia. Peroxisome proliferator activator receptors (PPAR) are key regulators of glucose and lipid homeostasis. We observed a striking downregulation of murine hepatic 11βHSD1 expression and activity after chronic treatment of wild-type mice with PPARα agonists, while 11βHSD1 in the livers of PPARα knockout mice, or in mice treated for only 7 h with PPARα agonists, was unaltered. Our results are the first to show PPARα agonists can affect glucocorticoid metabolism in the liver by altering 11βHSD1 expression after chronic treatment. Regulation of active glucocorticoid levels in the liver by PPARα agonists may in turn affect glucose metabolism, consistent with reports of their antidiabetic effects.

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    And this is why I have a tshirt with a picture of dsade on it. Gotta love the research.
    ~ Nothing can kill the Grimace!!



  3. NutraPlanet Fanatic
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    Quote Originally Posted by prld2gr8ns View Post
    And this is why I have a tshirt with a picture of dsade on it. Gotta love the research.
    And you know that t-shirt will always be nice and loose in the stomach area.

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    Awesome but I need to re read it at a computer! Thank you for this!

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    I didnt know that DCP required anymore studies!!! LOL

    Stuff absolutely rocks...


    Is the newer formulation without TTA going to be able to compete though? why the exclusion of TTA?
    iForceHemavol=He-man?-http://anabolicminds.com/forum/supplement-reviews-logs/187487-hemavol-heman-doughs.htmlCompound 20 Beta log-http://anabolicminds.com/forum/supplement-reviews-logs/185396-molding-dough-compound.html

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    The newer formulation includes ingredients that not only amplify mitchondrial activity directly, but increase PPAR expression - thus making the exclusion of TTA a moot point. PPAR agonism will be included still.

    TTA will be going the way of prescription medicine soon, and thus we won't be available to use it anymore.

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    wow... weird... I dont get how things that are once supplements get drafted into pharmaceutically exclusive...

    But thanks fr=or the response all the same!

    Im guessing you feel the new DCP r-i-v-a-l-s(wtfuh? why blank out *****?) the old formula? Would you say its more effective?


    ANNNDDDD.... if I have some TTA of my own... can I add it to the mix and not be creating a redundancy?
    iForceHemavol=He-man?-http://anabolicminds.com/forum/supplement-reviews-logs/187487-hemavol-heman-doughs.htmlCompound 20 Beta log-http://anabolicminds.com/forum/supplement-reviews-logs/185396-molding-dough-compound.html

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    You will absolutely be able to stock up TTA and add it to DCP 2.0.

    Right now we're just dealing with "on paper", but it looks like DCP 2.0 will be at least as effective as original DCP.

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    Quote Originally Posted by dsade View Post
    You will absolutely be able to stock up TTA and add it to DCP 2.0.

    Right now we're just dealing with "on paper", but it looks like DCP 2.0 will be at least as effective as original DCP.
    Im so stoked for DCP v2.
    E-Pharm Rep... PM me with any questions or concerns

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