Beyond Insulin?

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    Beyond Insulin?


    Thought this was interesting


    ScienceDaily (Apr. 3, 2012) New evidence points to a hormone that leaves muscles gobbling up sugar as if they can't get enough. That factor, which can be coaxed out of fat stem cells, could lead to a new treatment to lower blood sugar and improve metabolism, according to a report in the April issue of Cell Metabolism, a Cell Press publication.

    This new fat-derived hormone would appear to be a useful alternative or add-on to insulin; it can do essentially the same job, sending glucose out of the bloodstream and into muscle.

    "It's like you've opened the door and now the glucose can come in," said Jonathan Graff of the University of Texas Southwestern Medical Center.

    Graff's team manipulated a key developmental pathway in the fat stem cells of mice to find that the animals showed remarkably low blood sugar levels. The animals' muscles were taking up glucose at two to four times the usual rate thanks to an abundance of glucose transporters at their surfaces. That discovery was all the more striking because the animals also lacked fat stores, a condition known as lipodystrophy that normally results in just the opposite: high blood sugar and diabetes.

    The mice could respond normally to insulin, but insulin surprisingly had nothing to do with the muscles' unusual appetite for sugar. The source for the change wasn't anything inherently different in the muscle itself either; it was something about those manipulated fat stem cells.

    Further experiments revealed that the mouse muscles continued to take up extra sugar when they were isolated in the lab and exposed to blood serum. "It showed these effects were likely secondary to blood-borne signals sent by the manipulated fat cell progenitors," Graff says.

    That signal can be generated only by fat stem cells, not mature fat cells. When the researchers made the same developmental manipulation in adult fat cells, they saw no such effect on blood sugar or muscle.

    The findings highlight a new fat to muscle hormonal cue that would seem to have real therapeutic promise.

    "If we can purify this factor and give it to people, there is potential for its use to lower and help control blood sugar," Graff says. Alternatively, there might be a way to encourage fat stem cells in the body to produce more of the anti-diabetic factor themselves.
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    Reference for the article above

    Wnt Signaling Activation in Adipose Progenitors Promotes Insulin-Independent Muscle Glucose Uptake

    Summary

    Adipose tissues provide circulating nutrients and hormones. We present in vivo mouse studies highlighting roles for Wnt signals in both aspects of metabolism. β-catenin activation in PPAR-expressing fat progenitors (PBCA) decreased fat mass and induced fibrotic replacement of subcutaneous fat specifically. In spite of lipodystrophy, PBCA mice did not develop the expected diabetes and hepatosteatosis, but rather exhibited improved glucose metabolism and normal insulin sensitivity. Glucose uptake was increased in muscle independently of insulin, associated with cell-surface translocation of glucose transporters and AMPK activation. Ex vivo assays showed these effects were likely secondary to blood-borne signals since PBCA sera or conditioned media from PBCA fat progenitors enhanced glucose uptake and activated AMPK in muscle cultures. Thus, adipose progenitor Wnt activation dissociates lipodystrophy from dysfunctional metabolism and highlights a fat-muscle endocrine axis, which may represent a potential therapy to lower blood glucose and improve metabolism.
    http://www.cell.com/cell-metabolism/...131(12)00106-4
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    in for the read
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    bump
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    Insulin/Wnt crosstalk and wnt's effects on metabolism in general are becoming a hot topic. Insulin signaling regulates numerous Wnt pathway players and vice versa. Wnt also impacts gluconeogenesis, adipogenesis and appears to alter lipogenesis in some tissues.

    Problem is, wnt is a proliferative pathway, and disregulation of it is associated with various cancers.

    And just to clarify, what exactly the factor is in those PBCA mice is still unclear.
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    Quote Originally Posted by Resolve View Post
    Problem is, wnt is a proliferative pathway, and disregulation of it is associated with various cancers..
    As such, BigPaharma doesnt even have enough loot to get such a product past the FDA and on the shleves
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    Quote Originally Posted by Whacked View Post
    As such, BigPaharma doesnt even have enough loot to get such a product past the FDA and on the shleves
    Not yet anyways, though there is a lot of academic research being put into wnt inhibitors and hopefully partial agonists.
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    Simply taking a 1/4 teaspoon of cinnamon before meals can do wonders for your insulin also. Cinnamon is an insulin mimetic, meaning it has a similar structure to insulin so the body can use the cinnamon to perform the same function as insulin without having to release its won...ie, cinnamon helps the sugars get out of the blood and into the cells without insulin. It has been shown to improve insulin response up to 20 times normal, and was actually found out by accident when scientists were testing the effects of various foods on insulin levels. They tested the effect of apple pie and were dumbfounded when the insulin level actually dropped when they expected it to significantly rise. Thinking it was a mistake, the retested it and got the same result. They ended up finding it was the result of the cinnamon in the apple pie that was causing the insulin levels to drop.
  

  
 

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