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Today's News Stories: Leptin and Epigenetics

Discussion in 'The Leptin Rx' started by AKMan, Jul 3, 2012.

  1. AKMan

    AKMan New Member

    Why hasn't Jack told us any of this before???



    http://medicalxpress.com/news/2012-07-epigenetics-genes-rheumatoid-arthritis.html



    "A research team at the University of California, San Diego – led by Gary S. Firestein, professor in the Division of Rheumatology, Allergy and Immunology at UC San Diego School of Medicine – investigated a mechanism usually implicated in cancer and in fetal development, called DNA methylation, in the progression of rheumatoid arthritis (RA). They found that epigenetic changes due to methylation play a key role in altering genes that could potentially contribute to inflammation and joint damage. Their study is currently published in the online edition of the Annals of the Rheumatic Diseases.



    "Genomics has rapidly advanced our understanding of susceptibility and severity of rheumatoid arthritis," said Firestein. "While many genetic associations have been described in this disease, we also know that if one identical twin develops RA that the other twin only has a 12 to 15 percent chance of also getting the disease. This suggests that other factors are at play – epigenetic influences." "



    And: http://medicalxpress.com/news/2012-07-discovery-cellular-pathways-converge-food.html



    "The Kahn laboratory was the first to describe AMPK's critical role in mediating the actions of leptin, the hormone produced by fat cells that serves as a master regulator of neuroendocrine, metabolic, vascular, sympathetic and immune function. In 2002, Kahn demonstrated that AMPK is activated by leptin in skeletal muscle, thereby enabling the hormone to metabolize fatty acids. Subsequently, in 2004, her laboratory discovered that an opposing scenario takes place in the brain's hypothalamus, where AMPK is inhibited by leptin.



    "Having determined that leptin's effects on food intake and body weight depend on the inhibition of AMPK in the hypothalamus, we wanted to determine the signaling events that were responsible for this effect," she explains.

    "
     
    Da-mo likes this.
  2. KiwiLauren

    KiwiLauren Gold

    Love it... so glad to know that the Kahn laboratory was 'the first' to describe this and that I am therefore taking guidance from a figment of our collective imagination:)
     
  3. janagram

    janagram New Member

    help me out here...what are we talking aabout?
     
  4. AKMan

    AKMan New Member


    I was just trying to be funny. Both of these recent studies are talking about things Jack has been saying for years now.
     
  5. JoeBranca

    JoeBranca Silver

    I've been reading about epigenetics lately, and some of that in the article is making perfect sense to me. woo hoo
     
  6. janagram

    janagram New Member

    oh, duh. thanks...
     
  7. 2bls

    2bls New Member

    I figured you were being tongue in cheek...
     
  8. Jack Kruse

    Jack Kruse Administrator

    My entire blog is about this.........GO read the IF and leptin blog and tell me again that I have not told you about it? I did.......i dont think you got the message......because you did not have enough data points then to make sense of it. This is how the Quilt works.......when you dont know the science.......I need to give you small bites of it.......that is called a blog post. Then I slowly add more and more pieces to fill in the gaps. The more bits of knowledge you get your own brain puts things together and you have this insight or bolt of intuition that maybe I might be correct. When bits of knowledge come together we call this wisdom. Wisdom and knowledge are not the same........knowledge does not always lead to understanding. If you do not believe that go read a scientist blog like Guyenet. There they argue constantly about bits of knowledge instead of putting the knowledge together into a framework of how it works.........for an organism. I do the opposite. Guyenet is a 30 ft guy (and he is quite smart by the way, but being smart can also allow you to fall thru many trap doors when your vision is constricted by facts not connected to a wisdom)........



    I am a person who gets the 30 ft perspective but I connect the dots to get the 30000 ft view before I use it. Why? If I am wrong, I can get sued.......Guyenet can't, and he just goes on to another experiment.



    This is why I have to really think in 6 dimensions to make sure things are safe before we apply them...........physicians and surgeons operate on the 30000 ft to help disease and wellness........But if some of the bits of knowledge we accept and acquire are off........the 30000 ft view is off (think cholesterol or Hormones as a great example) I hope this makes sense..........
     
  9. janagram

    janagram New Member

    I didn't realize AKman was being facetious....but, yeah, he realizes you HAVE told us this!

    And thanks for this further discussion, because it is very interesting. I really appreciate the 30000 foot view....the 30 ft. view is just news I can't use! And I like the way you discriminate between wisdom and knowledge....very important.
     
  10. Michalis

    Michalis New Member

    I am really late to the party but things have started making sense a bit.

    For the folks like me that were or still are obese and have cartilage issues see the links below.. Leptin and Cartiladge... Boom.


    http://ard.bmj.com/content/71/3/455

    Conclusions Leptin acts as a pro-inflammatory adipokine with a catabolic role on cartilage metabolism via the upregulation of proteolytic enzymes and acts synergistically with other pro-inflammatory stimuli. This suggests that the infrapatellar fat pad and other WAT in arthritic joints are local producers of leptin, which may contribute to the inflammatory and degenerative processes in cartilage catabolism, providing a mechanistic link between obesity and osteoarthritis.


    http://onlinelibrary.wiley.com/doi/10.1111/bcpt.12160/full

    Conclusions
    In the light of the presented evidence, obesity as a risk factor for OA turns out to be more than just weight loaded on joints. Adipocytokine leptin emerges as a potential obesity-related systemic factor that could push intra-articular balance towards inflammation and destruction in the pathogenesis of OA. The whole pathophysiological network of OA involves multiple mediators, but obese OA patients seem to be more susceptible to the detrimental effects of leptin in the joints because of elevated levels of bioactive leptin in the synovial fluid and, further, due to increased responsiveness of the cartilage to the leptin effects when SOCS-3 levels are low (figs 2 and 3). The evidence discussed in the present MiniReview supports the idea of leptin as a possible link between obesity and OA, and as a target for disease-modifying drugs for the treatment for OA.


    This one as well might have been posted in the forum somewhere..

    http://www.tandfonline.com/doi/abs/10.1080/03008207.2017.1385605?journalCode=icts20

    Abstract :
    Leptin alone and in combination with interleukin-1-beta induced cartilage degradation potentially inhibited by EPA and DHA
     
    Da-mo likes this.
  11. Sandy palardy

    Sandy palardy New Member

    Still spinning info around
     

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