What happens to glucose forced into fat.

Animalkits

Community Veteran, Conversion Kits Pioneer
This question has been asked over and over again, yet never an answer.

Hopefully somebody ELSE will present it so we all know.
 
Add to that how long ALA stays in the bloodstream so if used to dispose glucose you will know EXACTLY down to the second how long you have when you eat.

(chances are you are entirely MISSING the insulin rise.)
 
Chirp!

It's not long enough for some studies and nobody tells you how long, do they?
 
niether ala nor r-ala "forces" glucose into fat.

thats a concept you made up in your mind.

peak plasma is reached within 1/2 hr of admin, half life estimates (from peak) run from 30-90min (research is on going in this area)
 
Animalkits said:
This question has been asked over and over again, yet never an answer.

Hopefully somebody ELSE will present it so we all know.

MAC...with ALL due respect (and let it be known that I have taken ala and r-ala for years and believe it to be effective at GLUCOSE CLEARANCE), this question needs to be addressed regardless of the your feelings for the author.

After the excessive carbs/glucose to cleared from the bloodstream, how can we be sure it does NOT go into the adipocyctes? Thru ALL the arguing of late, THIS question (originally asked by ME anyway if that makes you feel better) has been unaddressed. Afterall, w/o exercise, the glucose should have NO preferential depositing of the skeletal muscle or the fat tissues. So WHAT mechanisms support the preferential directing of glucose into the skeletal sites as opposed to the fat ones?

I do see Animal's point .........if the excess is in fact directed into the adipocytes, that is a problem (albeit still not as big a problem of the raised insulinemia).

Thank you (and I am on NO ONE's side in this ongoing argumnent here for the record LOL......only wanting an answer thats all)

Animal/Mac....Mac/Animal.........KEEP THIS CIVIL!!!! :mad:
 
As far as increase in adiposity this has been directly addressed on three counts:
1. r-ala lowers plasma insulin response (both directly through action on pancreas and through glucose clearance)
2. r-ala inhibits adipogenesis via the MaPK pathway and ppar-y antagonism
3. animals treated with r-ala show decreases in adiposity, both lean and obese models.


btw- if fat cells are insulin resistant, as noted in the glut-4 study cited in the IGF-1 thread, the result is poor glucose clear, hypergylcemia and adiposity. as a note if your fat cells were to lack an insulin receptor as that FIRKO mice did the effects are increased insulin sensitivity in both muscle and the fat tissues that they do have.

as a further note all cells store glycogen and utilize glucose, even adipocytes, in fact their uptake of glucose increase leptin levels.
 
macro said:
As far as increase in adiposity this has been directly addressed on three counts:
1. r-ala lowers plasma insulin response (both directly through action on pancreas and through glucose clearance)
2. r-ala inhibits adipogenesis via the MaPK pathway and ppar-y antagonism
3. animals treated with r-ala show decreases in adiposity, both lean and obese models.


btw- if fat cells are insulin resistant, as noted in the glut-4 study cited in the IGF-1 thread, the result is poor glucose clear, hypergylcemia and adiposity. as a note if your fat cells were to lack an insulin receptor as that FIRKO mice did the effects are increased insulin sensitivity in both muscle and the fat tissues that they do have.

as a further note all cells store glycogen and utilize glucose, even adipocytes, in fact their uptake of glucose increase leptin levels.

Ok, I am in accord with the argument that r-ala/ala has the ability to lower blood glucose levels hence, lower insulin levels as well.
The fact that insulin has a fat-sparing effect, as it drives most cells to preferentially oxidize carbohydrates instead of fatty acids for energy, and indirectly stimulates accumulation of fat is adipose tissue...supports the argument FOR r-ala/ala.

However....

We know that Insulin facilitates entry of glucose into muscle and ADIPOSE (and several other tissues). The ONLY mechanism by which cells can take up glucose is by facilitated diffusion through a family of hexose transporters. In muscle tissues - the major transporter used for uptake of glucose (GLUT4) is made available in the plasma membrane through the action of insulin. SO.......in theory, if insiulin levels have been lowered as a direct result of the r-ala/ala...GLUT4 is inhibited - result: inability to uptake glucose into the MUSCLE cells----very bad!!!!

Essentially, the GLUT4 glucose transporters are useless for transporting glucose in the event glucose has been cleared and insulin levels have dropped.

(Obviously the liver/brain requirement is a NON-issue as they have an efficient means of glucose uptake (independent of GLUT4) of glucose/ATP synthesis).

In the absense of insulin, a bulk of the cells in the body become unable to take up glucose, and begin a switch to using alternative fuels like fatty acids for energy; which is obviously what we want as far as shifting our bodies into lipolysis anyway. However, introducing ala + carbs/glucose; changes this scenario to a degree.

Let's say (for argument's sake) that the excess glucose is directed towards glycogen stores vs fatty acid synthesis....when the liver is finally saturated with glycogen, any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids anyway (as lipoproteins). UNDESIRABLE. :confused:
 
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I asked about this when ala first came out, I never did get a satisfactory answer form anybody I asked. I asked about chromium GTF as well as ala, "what happens when the liver and muscle are glycogen loaded?'
It gets excreted as waste? ..... I think that's the only way it would make sense,,,and that doesn't make sense...by what pathway
 
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