Fat or Muscle: How does lipoic acid know?

[smokinghawk]

ALa helps with glucose disposal--we all know that by now. But how does it know where to preferably "send" glucose--to muscle, rather than to fat? Why would it not just shuttle glucose into fat cells like any other, and what gives it its partitioning abilities?

 

[macrophage69alpha]

according to most research.. it does not..

but users results seem to fly in the face of this...

it may be more a matter of increasing sensitivity. reducing presence of insulin (which blunts GH effects)..

thus it may work more by "helping" GH. (at least from the fat loss perspective)

as to preferential shuttling ??? though users do "seem" to report this as well..

 

[plornive]

It works because less glucose gets to the liver and more gets to the muscles. Glucose transport enzymes on fat mean some glucose will go to adipocytes, but as a result less will get to the liver. This is what is important since liver glycogen can very easily be converted to free fatty acids. You should try to mobilize your own fat stores instead of creating them from glucose in the liver.

If you didn't use ALA, less glucose would be pushed into adipocytes but also less in muscle cells and more in the liver. The end result is that ALA will help partition nutrients away from fat storage.

 

[plornive]

it may be more a matter of increasing sensitivity. reducing presence of insulin (which blunts GH effects)..

ALA will truly not affect the amount of insulin released very much. If it did, then blood sugar would not be lower as a result of ALA use. This is confirmed in studies.

 

[BackDoc]

Let me see if I can shed some theoretical light on the subject.

ALA may act as a co-conspirator (so to speak) with existing (normal) levels of insulin. At 600 mg doses (until it is cleared from the system) ALA will add to the glucose uptake previously only handled by insulin. However, since there are selective tissues that will allow ALA mediated glucose uptake metabolically active tissue is one way of preventing problems with glucose disposal. This explains why diabetics on ALA will still have ketosis readings but yet have greatly diminished urinary sugars and somewhat normalized blood glucose readings.

Insulin works the way it does for very good reason. Insulin is the "key" molecule that allows glucose to enter most cells of the body. Without insulin, glucose sits in the bloodstream. This is why diabetics (who do not produce insulin) have problems with rapid onset, rapid progression of infection: bacteria consume sugar also and as blood glucose stays high, bacteria feed and proliferate more so than normal. Thus there is a feeding ground for all the nasties that can lead to tissue damage and disease morbidity at the slightest chance.

Since ALA does not radically alter insulin secretion it could also be theorized that there is still a yet unidentified interaction between ALA and insulin. By working on glut 4, receptors, etc, ALA allows muscle cells to take in more glucose (which can be assumed without research to nullify) that since there is no modification of insulin when ALA is consumed that it could be merely enhancing the work of insulin rather than functioning similarly and separately. If ALA did work similarly but separately, then we could expect to see some sort of insulin secretion response perhaps by a negative feedback loop that the body is so prone to do in the first place. There are no free lunches in the body when dealing with hormone manipulation. This is why I feel I can theorize that ALA does not particularly function similar to insulin but rather may modify the environment to the extent that insulin function remains normal and even enhanced.

This brings up the theory as to why would diabetics with reduced or absent insulin secretion benefit at all with ALA addition...in such case ALA may function partially in conjunction with insulin to enhance it, or it may function as a weak alternative. Sort of like Echinacea...enhancing an alternate pathway. In the case of ALA it may be working through a particular pathway that is yet unknown/not realized. In this situation it would explain why it does not alter insulin levels significantly yet seems to increase glucose uptake in some tissues.

The reason why I don't believe ALA is doing much in terms of adipocyte storage increase is that if glut 4 myocyte modification is going on the body will manufacture necessary glucose to fill the gap that diet cannot fulfill in steady stages. As the glut 4 modification is going on the body will work in a positive feedback loop and make the most of the fact that glut 4 modification will allow more muscle glycogen storage without the burden of increased glycation of proteins. This makes a good theory explaning why some people tend to be lower in ketosis immediately following a meal (just a few minutes) in which ALA was taken, yet have very high ketosis a few hours later.

 

[macrophage69alpha]

actually since there are virtually no studies in NON DIABETICS.. it is hard to say what its effects are..

especially at the doses being used here and in conjunction with various other drugs..

also due to the nature of ALA and it short half life.. frequent dosing may be necessary... there are few studies that have used multiple dosing.. none of the study dosages are close to what is now being used.. and those in the studies were diabetics...

 

[BackDoc]

Exactly, and I agree completely. In this case, since few, if any, non-diabetics were subjects, except in a few cases where the control group were composed of some non-diabetics, the data does not translate well into the ramifications for the non-diabetic. What the literature does seem to indicate is that there is no negative feedback loop with regards to insulin and ALA use. From what I can find, there is a dose limit of 600 mg and normalization of glucose. That is, at a dose higher than 600 mg there is neither increased or decreased benefit (short of doses approaching the LD50). So when discussing the effects of high dose ALA, the insulin question is pointless comparing diabetics to non-diabetics.

There is one study of 1800 mg per day that did not report any unusual side effects. For this study it confirmed that with increased dose of ALA there is another perhaps unknown mechanism via which ALA is functioning. In this case, assuming there are no other pathological conditions present in the study group, it does bring up the question of decreased glycation and increase myocyte uptake of glucose. Some ridiculously incomparable animal studies have shown this but it will be nice to see it with higher primates, or even some Italian human studies.

 

[smokinghawk]

Thanks--and a question to clarify this for me.

One message above swaid thatresearch says it doesn't, although anecdotal evidence fomr users is different.

But another message pointed out that ALA works on the Glut4 receptors in muscle, which is why muscle gets top-preference for blood glucose from ALA's actions. Does this happen because ALA increases the number of muscle cell receptors to glucose, or does ALA simply make existing receptors more sensitive?

 

[BackDoc]

I would assume that it is a receptor mediated response; the cell membrane responds to allow greater glucose uptake in whatever form whether accompanied by insulin or ALA or both. I know that neither explains the glut 4 interaction nor the decrease in glycation, so all we can do is speculate until further research determines the specific pathway.