INSULIN RESISTANCE


   FIRST OF ALL WE NEED TO KNOW WHAT INSULIN IS AND HOW IT WORKS:-


     WHAT IS INSULIN 


  • INSULIN IS A KEY HORMONE REGULATING GLUCOSE HOMEOSTASIS

         (STABLE STATE).

  • IT'S MAJOR TARGET TISSUES ARE THE LIVER,THE SKELETAL

       MUSCLE AND THE ADIPOSE TISSUE.

       INSULIN KEEPS YOUR BLOOD SUGARS FROM GOING TOO HIGH.

  •  SO,BASICALLY INSULIN PREVENTS THE BLOOD SUGARS FROM GOING   BEYOND A CERTAIN LEVEL
  •                                                                      AROUND (< 130 mg/dL).


     MECHANISM 


  • WHAT WE TYPICALLY THINK OF INSULIN AND INSULIN RECEPTORS AS A LOCK AND KEY MODE i.e, INSULIN IS LIKE A KEY AND THE RECEPTOR IS LIKE A LOCK.

  • SO INSULIN WHEN IT GOES UP AFTER YOU EAT, OPENS UP THE LOCK AND LETS GLUCOSE INTO THE CELL.



      





       FULL ARTICLE
 

     What we typically think of insulin and insulin receptors as a lock and key model that is, insulin is like a key and the receptor is like a lock. 

  So insulin when it goes up after you eat opens up the lock        and lets glucose into the cells.

  So during insulin resistance what happens is that we see that there's lots of insulin around but yet the glucose is not going into the cell so classically we believe that there must be something gumming up this mechanism .

  You can clone the receptors and you can see that they're all  normal you can see that the insulin molecule is normal so it's not like the key is deformed and it's not like the the lock is deformed those are both normal.

   
       But perhaps there's something like a piece of gum that's
   just sitting in that lock that's preventing it from working and      because it doesn't work the glucose piles up on
  the inside and it's classically understood to have nothing on      the inside or if the cell is facing internal starvation.
                   But the problem with that sort of paradigm is that if you look at type-2 diabetes these people don't look like they're starving in fact there's excess fat everywhere they have too much body fat but they also have way too much liver fat they have too much visceral fat so it doesn't really jive if you have type 1 diabetes which is the severe lack of insulin there you do face a situation of internal starvation.


   But if you look at the kids who develop this disease they are skeletal, they really cannot put on weight no matter what. So
that's real internal starvation and  type 2 is nothing like that.
      
     So we know that this sort of paradigm is incorrect because   there's actually a paradox that's not often talked about so this   is the central paradox of insulin resistance.
    
    That is insulin resistance means that your body should be resistant to the effect of insulin so we see that because the glucose does not go up the other thing insulin does is that it
promotes the storage of body fat.
     
       Remember when you eat insulin goes up you store food energy some of it as fat.

   
     When you have type 2 diabetes which is a disease of very high insulin resistance, what happens is that your body should because it's resistant to the effect of insulin not be producing
any fat.
          So if it's in a state of internal starvation it shouldn't be making any new fat but that's not true.
     We know that in type 2 diabetes people have big fatty livers and they're producing huge amounts of new fat so here's the paradox, if the cell has no glucose on the inside how can it produce fat from that glucose there is none 

   It's like trying to build a house with no bricks, you might have all the carpenters and all the construction workers but if you have no bricks you can't make it.
So how are you going to make these new molecules of fat if you have no glucose to make them and there's no substrate so that's the paradox of insulin resistance, and 

one effect of insulin which is letting the glucose in is resistant 

but the other effect which is making these new fat cells is not resistant it's actually accelerated,
    so at the same time in the same cell with the same insulin with the same insulin receptor one effect is resistant and once one effect is accelerated.
     So the entire paradigm does not work so what you have to
understand is that insulin resistance is neither a broken lock and nor gummed up locking key.


So the question is what it really is;

 It's an overflow mechanism so if you have insulin and it's trying to push this glucose into the cell there's another
possibility why this glucose isn't going in and this is that
 there's just too much in there.

LET ME GIVE YOU AN ANALOGY SO THAT YOU CAN UNDERSTAND BETTER


     So if you think about packing a suitcase when you put your
luggage in at first ,it goes nice and easy but once it's full it's really hard to shove those last two t-shirts into your suitcase and it's not because there's anything wrong with the suitcase or with your t-shirt ,it's simply because there's just too
much.

So that's what's happening in the state of insulin resistance is that your cell is so full of glucose that it won't push anymore in.
At the same time that liver cell is desperately trying to make
new fat and shuttle it out somewhere else, 
shuttle it out the other side and that's what really insulin resistance is.


        So if you understand that insulin resistance is really the effect of too much insulin for too long and too much sugar, then again the solution becomes extremely obvious what you don't want to do is keep pushing in more t-shirts into that suitcase.
         What you want to do is get rid of that, you need to get rid of the sugar.


    And that's a dietary issue not a drug issue.
           

It's not like we're trying to fix the receptor it's just too much sugars sitting inside the cell.
 That's it.


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