Sunday, 29 April 2012

What if fat works like muscle?

This post probably wont make any sense, I am slightly psychotic, you know.

Myostatin is a negative regulator of muscle growth. Without Myostatin your muscles will grow huge, regardless of anything else you do. Another requirement of muscle growth is "activation". I.E. the old phrase, use it or lose it. Muscle activation commences by the nervous system, so the more nervous system stimulation you give to muscle, the more it will grow. There does seem to be one other factor though as EMS ( electrical muscle stimulation ) is not quite as effective as exercise by the host organism. I have no idea personally what the missing ingredient is though.

A clue to the mechanism of Myostatin control of muscle growth comes from this recent paper, it looks like myostatin deficiency allows for greater nervous system innervation of the muscle. This makes sense, because as stated above, the number 1 rule governing muscle mass is nervous system stimulation ( activation ).

Adipose tissue is also innervated by the nervous system, and this innervation ALSO seems to be critical for managing adipose tissue mass. Further, denervation of fat tissue increases fat pad mass and fat cell number ( 1 ). I didnt see anything mentioned about calories in calories out there btw....

Having recently brought myself up to date on the latest model we have for lipolysis, it seems that the current mainstream view of "insulin inhibits fat breakdown by stopping hormone sensitive lipase" is actually VERY crude and sketchy. The truth is its wwaaaayyyyy more complicated than that.

The latest model of lipolysis involves atleast 3 different enzymes. Triglyceride inside fat cells is trapped inside a lipid droplet. To begin lipolysis, the triglyceride is first acted on by an enzyme called adipose triglyceride lipase ( ATGL ) , this converts it to diglyceride, which is 2 fatty acid molecules attached to glycerol. Once its a diglyceride, ATGL becomes useless and we next have to make use of our old friend hormone sensitive lipase.

HSL is responsible for further chopping the diglyceride into monoglyceride, after which it is acted on by another enzyme to finally break it down into fatty acids + glycerol. The twist in the tale is that HSL is actually under neuroendocrine control. HSL activity is low until stimulation of the fat cell by the nervous system. And norepinephrine is the signal molecule acting via the nervous system.

So basically, HSL is not only negatively regulated by insulin, it is also positively regulated by norepinephrine. And surprise surprise, obese people have low rates of HSL activity via norepinephrine stimulation ( 2 ). By the way, women with PCOS also have reduced HSL activity, although it doesnt appear to be as bad as in obesity.

But this brings us back to the serum FFA paradox, if obese people have low rates of lipolysis via low nervous system stimulation of HSL, why do they have increased circulating FFA?

As I said, its a paradox.

The bottom line and point im trying to make here is that, fat tissue mass is principally controlled by nervous system stimulation just as is muscle tissue mass. I also personally speculate that, just like muscle tissue mass will grow to extreme levels without negative feedback from Myostatin, fat tissue mass will also grow to extreme levels without negative feedback from X.

What is X? fuck knows lol. Let the so called medical industry figure it out, its not my job, im just an average guy who works in I.T.

But, if you really want my opinion, I think that MC4R is a big part of X.

MC4R also acts on fat cells via the nervous system ( 3 ). It was slightly painful to read in that paper that "pale skin" was associated with mutations in the neuroendocrine system, as I have been "slightly" chubby my entire lift and also suffer from pale skin. It is very white, and I NEVER EVER tan in the sun, no matter how long I spend in it.

1 comment:

  1. how VERY interesting! i expect you to have solved the puzzle by the time i get home from my trip.... ;-)