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PROLOR Biotech, Inc. Message Board

  • clausonwill clausonwill Nov 28, 2012 9:18 AM Flag

    Oxyntomodulin races heart. that is vvus's problem with q. it is dead on arrival

    Oxyntomodulin will be dead on arrival. this is the term to look at-- "significantly increased HR"
    good luck. you should look at arna, it is going over 50 next year and at 9 now. it has been approved and does not race the heart.

    The cardiovascular effects of OXM were examined in conscious and freely moving mice. Peripherally administered OXM significantly increased HR in wildtype mice, and even in Glp1R -/- mice. Hence OXM modulates murine intrinsic HR through a GLP-1R independent mechanism, perhaps via the glucagon receptor or an unidentified OXM receptor. See Oxyntomodulin increases intrinsic heart rate in mice independent of the glucagon-like peptide-1 receptor. Am J Physiol Regul Integr Comp Physiol. 2006 Oct 12;

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    • Oxyntomodulin increases intrinsic heart rate in mice independent of the glucagon-like peptide-1 receptor.
      Sowden GL, Drucker DJ, Weinshenker D, Swoap SJ.
      Source

      Department of Biology, Williams College, Williamstown, MA 01267, USA.
      Abstract

      Oxyntomodulin (OXM), a postprandially released intestinal hormone, inhibits food intake via the glucagon-like peptide-1 receptor (GLP-1R). Although OXM may have clinical value in treating obesity, the cardiovascular effects of OXM are not well understood. Using telemetry to measure heart rate (HR), body temperature (Tb), and activity in conscious and freely moving mice, we tested 1) whether OXM affects HR and 2) whether this effect is mediated by the GLP-1R. We found that peripherally administered OXM significantly increased HR in wild-type mice, raising HR by 200 beats/min to a maximum of 728 +/- 11 beats/min. To determine the extent to which the sympathetic nervous system mediates the tachycardia of OXM, we delivered this hormone to mice deficient in dopamine-beta-hydroxylase [Dbh(-/-) mice], littermate controls [Dbh(+/-) mice], and autonomically blocked C57Bl mice. OXM increased HR equally in all groups (192 +/- 13, 197 +/- 21, and 216 +/- 11 beats/min, respectively), indicating that OXM elevated intrinsic HR. Intrinsic HR was also vigorously elevated by OXM in Glp-1R(-/-) mice (200 +/- 28 beats/min). In addition, peripherally administered OXM inhibited food intake and activity levels in wild-type mice and lowered Tb in autonomically blocked mice. None of these effects were observed in Glp-1R(-/-) mice. These data suggest multiple modes of action of OXM: 1) it directly elevates murine intrinsic HR through a GLP-1R-independent mechanism, perhaps via the glucagon receptor or an unidentified OXM receptor, and 2) it lowers food intake, activity, and Tb in a GLP-1R-dependent fashion

 

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