Unfortunatelty.....the OTHER ala thread was closed so......

[Animalkits]

And here is the problem and it's with muscle in diabetics and inhibition of glycogen synthesis! The problem isn't with making fat cells LESS insulin resistant, but MUSCLE!

Determining the Rate-Controlling Step for Insulin Stimulation of Muscle Glycogen Synthesis
Insulin resistance in patients with type 2 diabetes can mostly be attributed to decreased insulin stimulation of muscle glycogen synthesis, and defects in glycogen synthase, hexokinase, and glucose transport have all been implicated as responsible for the lower rate of glycogen synthesis. To determine the relative importance of each of these steps in muscle glucose uptake and metabolism, we used a 13C/31P NMR approach to measure intracellular concentrations of glucose, glucose-6-phosphate (G6P), and glycogen in muscle in patients with type 2 diabetes and in normal subjects. Because it has been proposed that decreased delivery of insulin to the muscle underlies insulin resistance in type 2 diabetes, we also measured insulin concentrations in interstitial fluid.

 

[Animalkits]

Ima learnin myself a sumptin.

 

[Animalkits]

Better cut out the fat, too which is one of the HUGE probs with those ketogenic diets.

Serine Kinases and the Pathogenesis of Fat-Induced Insulin Resistance
The mechanism by which lipid infusion causes insulin resistance in skeletal muscle may involve increases in intracellular FA-derived metabolites (e.g., fatty acyl CoA, diacylglycerol, ceramides) and subsequent activation of a serine/threonine kinase cascade involving protein kinase C-q (PKCq) and IkB kinase b (IKKb). We have shown that an acute elevation of plasma FAs for 5 hours results in activation of PKCq, which is associated with decreased tyrosine phosphorylation of IRS-1. This decrease may involve serine phosphorylation of IRS-1, proteasome-mediated degradation of IRS-1, or phosphatase-mediated dephosphorylation of IRS-1.

 

[macro]

And here is the problem and it's with muscle in diabetics and inhibition of glycogen synthesis! The problem isn't with making fat cells LESS insulin resistant, but MUSCLE!

Determining the Rate-Controlling Step for Insulin Stimulation of Muscle Glycogen Synthesis
Insulin resistance in patients with type 2 diabetes can mostly be attributed to decreased insulin stimulation of muscle glycogen synthesis, and defects in glycogen synthase, hexokinase, and glucose transport have all been implicated as responsible for the lower rate of glycogen synthesis. To determine the relative importance of each of these steps in muscle glucose uptake and metabolism, we used a 13C/31P NMR approach to measure intracellular concentrations of glucose, glucose-6-phosphate (G6P), and glycogen in muscle in patients with type 2 diabetes and in normal subjects. Because it has been proposed that decreased delivery of insulin to the muscle underlies insulin resistance in type 2 diabetes, we also measured insulin concentrations in interstitial fluid.

there are a dozen studies that say otherwise. its really a mistake for them to make the conclusion that they have because all insulin resistance will slowly lead to increased plasma insulin which lowers insulin receptor responsiveness. There are also other factors. there are plenty of lean type II diabetics (they are not the masses, but they are a significant population).

 

[ulter]

"there are plenty of lean type II diabetics (they are not the masses, but they are a significant population)."

Animal if you can find out why this is you'll win the Nobel Prize.
No one knows what causes insulin resistance. Natives of the sub-continent develope adult onset diabetes after an increase of only 2kg in body fat. While some Angelo's, Euro's, can gain 60 pounds and not become insulin resistant or develop Type 2.
What is known is that R+ Lipoic acid is present in traces in the mitochodria of the muscle cells and slowly disappears with either age, the use of AS and poor eating habits, in some people.
If you give a bowl of ice cream to a 2 year old they will be bouncing off the walls in 30 minutes. If you give the same ice cream to someone 40+ or a body builder who has been cycling they go take a nap on the couch. There is your classic demonstration of insulin resistance and in both the 40+ and the BBer R+ Lipoic acid will change that outcome because this group doesn't have their natural R+ Lipoic Acid that fires up the mitochondria anymore.
Like Macro keeps saying if you reduce the plasma insulin you'll reduce the fat. If you fire up the mitochondria in the muscle cells with R+ Lipoic Acid they will take in more glucose and will lower your plasma insulin levels. Which in turn lowers your fat.
See http://www.anabolicfitness.net/ALA/index_1.htm

 

[ulter]

"Please post their signed affidavits."
Glucorell R had to be approved by these physicians and pharmacists before it could be added to the "catalog" of AARP and AmeriMark. It's been approved for both catalogs. AmeriMark, again, is the worlds largest medical supply catalog in the US and you know who AARP is.

"Researchers are the same as doctors?"
Usually a researcher has a PhD. No?

 

[Animalkits]

In another thread we were discussing the similarity of ALA to IGF from some info I posted, however, I have some problems with those mechanisms in the study as their end conclusion as did some of their citations.

Anyhow, it was said that IGF works in a way similar to ALA and even that ALA would increase fat burning aside from the lowering of insulin.

However, nobody I know of anywhere be they close personal friends or elves or whomever who would EVER say that ALA is anything similar to IGF.

Somebody also said insulin resistance in fat is bad since muscle only makes up a small amount of glycogen stores, nevertheless, insulin resistance in fat in mice has been shown to NOT affect overall glycogen syn.

In the first study, Kahn and colleagues bred mice to lack the insulin receptor in their fat cells. These animals are called fat-specific insulin-receptor knockout (FIRKO) mice. This work exploited the Cre–lox technology for tissue-specific disruption of protein expression, which is a powerful approach to analyse complicated and interacting biochemical pathways. FIRKO mice had a lean body mass and differed from control mice in that they were protected from obesity associated with age or overeating. Importantly, they were also protected from developing obesity-associated or age-related insulin resistance, which leads to diabetes. Interestingly, FIRKO mice had two different populations of adipocytes, small and large, which differ in expression of the enzyme fatty-acid synthase and the transcription factors C/EBP (CCAAT/enhancer binding protein-) and SREBP1 (sterol-regulatory-element-binding transcription factor 1). It is thought that loss of the adipocyte insulin receptor unmasks differences between two sizes of fat cell and that the small adipocytes are somehow protected against excessive fat loading, preventing the mice from becoming obese. Although FIRKO mice show insulin resistance in the adipose tissue, whole-body glucose metabolism is not affected.

We still have the problem of what happens to glucose when it goes into fat cells. They aren't glycogen repositories so there is only really one metabolic pathway which hasn't been answered.

 

[Animalkits]

BTW, if you are pushing glucose into muscle and fat since glycogen stores are only 20% in muscle, that leaves 80% jamming into liver and fat.

THAT'S A BLOCKBUSTER!

 

[TxLonghorn]

What is known is that R+ Lipoic acid is present in traces in the mitochodria of the muscle cells and slowly disappears with either age, the use of AS and poor eating habits, in some people.

This is interesting.

Btw, thank you animal, macro, and ulter for keeping this discussion about the facts and questions presented.

 

[macro]

no animal, its not.

liver and muscle have the greatest ratios percentage wise
1-2% of muscle weight
10-12% of liver weight

all the tissues of the body store glycogen to one degree or another. including RBC's and leukocytes.

it is also important to note that up to 75% of the glucose used in the day is used in the brain, R+ lipoic and ALcar have been shown to increase metabolic rate in brain tissue, restoring mitochondrial activity (the Ames study)

glycogen is also stored in BAT and to small extent other types of adipose tissue.

and its important to also note that 3T3-L1 adipocytes are more efficient at the uptake of glucose than human adipocytes.

finally the effects of r+ lipoic on clonal expansion and pre-adipocyte differentiation.. means that these cells do not become fat cells they are either lysed or utilized for energy. Mature adipocytes produce several factors, including pge2, which inhibit lipolysis (these cells are resistant to energy utilization).
^
^
^
what this means that is in caloric excess you will not get AS fat as you would otherwise. It also, likely through several mechanisms possibly including carbohydrate oxidation, increases mean metabolic rate

 

[TxLonghorn]

Ok, lemme see if I can dummy this down so I can understand this...'cause you guys kinda lost me there...

Let's say you take in excess carbs...the breakdown of carb/glycogen storage is muscle, liver, rbc's, fat cells, etc. with most carb/glycogen usage being the brain. Right?

Now, what is done with the excess carbs usually? Turned into fat, right? We get an insulin burst, some of the energy is lost in the transformation, but we basically get fatter, right?

Now take the same excess and add r-ala to the mix...we don't get as fat, and possibly get leaner (as long as the excess is not too much) because...? Because of increased oxidation? Other mechanisms? Do we have some clue as to how much leaner? This is the part that loses me.

 

[WI]

Ok, lemme see if I can dummy this down so I can understand this...'cause you guys kinda lost me there...

Let's say you take in excess carbs...the breakdown of carb/glycogen storage is muscle, liver, rbc's, fat cells, etc. with most carb/glycogen usage being the brain. Right?

Now, what is done with the excess carbs usually? Turned into fat, right? We get an insulin burst, some of the energy is lost in the transformation, but we basically get fatter, right?

Now take the same excess and add r-ala to the mix...we don't get as fat, and possibly get leaner (as long as the excess is not too much) because...? Because of increased oxidation? Other mechanisms? Do we have some clue as to how much leaner? This is the part that loses me.

Bump it up for Tx's questions, I'm a little confused myself but willing to learn!

 

[Drveejay11]

Ok, lemme see if I can dummy this down so I can understand this...'cause you guys kinda lost me there...

Let's say you take in excess carbs...the breakdown of carb/glycogen storage is muscle, liver, rbc's, fat cells, etc. with most carb/glycogen usage being the brain. Right?

Now, what is done with the excess carbs usually? Turned into fat, right? We get an insulin burst, some of the energy is lost in the transformation, but we basically get fatter, right?

Now take the same excess and add r-ala to the mix...we don't get as fat, and possibly get leaner (as long as the excess is not too much) because...? Because of increased oxidation? Other mechanisms? Do we have some clue as to how much leaner? This is the part that loses me.

THIS is precisiely where the controversy begins and has been rebuttled to death here; unfortunately w/o a conclusive and convincing answer.

Animal's claims: ALA/r-ALA "jams the the "excess" carbs (glucose) into adipocytes (fat cells) as storage making you fatter.

Mac/Ulter's claim: ALA/r-ALA "jams the the "excess" carbs (glucose) into skeletal muscle and glycogen stores (avoiding adipocytes) making you leaner.

Seems as if all parties are in accord that the R-ALA/ALA fascilitates the movement of carbohydrates out of the bloodstream.......it's the preferential "landing" location that is being contested here, and FOR GOOD REASON!!!

 

[Animalkits]

They also claim that only 20% of glycogen stores is muscle.



100% minus 20% is 80%. Simply said, 80% of the glucose is going into fat as ALA has no preference for muscle over fat and fact is that FAT would greatly outcompete muscle at grabbing it at a 4 to 1 ratio.

'Mac/Ulter's claim: ALA/r-ALA "jams the the "excess" carbs (glucose) into skeletal muscle and glycogen stores (avoiding adipocytes) making you leaner.'

 

[ulter]

The reasons why Glucorell R works so well are more complex than just where the glucose goes. Although Glucorell R will cause the mitochondria to make the muscle cells uptake more glucose than normal the most significant fat loss comes from it's ability to lower your plasma insulin levels. These levels are higher than what is healthy, in those who are insulin resistant. If you're not insulin resistant then most of the glucose uptake benefits of Glucorell R will not be as prominent. The problem is that most of us ARE insulin resistant and that's why most of the people on the Anabolic Boards and Diet Boards see such great results from Glucorell R regardless of where the glucose goes.
But Macro has more to say on the "disappearing glucose trick". Hint: It doesn't matter where it goes...

 

[Drveejay11]

"Hint: It doesn't matter where it goes..."

That just isn't right bro..............LOL.

 

[Animalkits]

Oh, I see, most of the population is now insulin resistant, too!

I guess if your customers are such pigs that they keep eating glucose when they have enough energy already, they kinda deserve what they get.

Still if they are in a constant state of piggery, they are still gonna be fatter.

Unless of course you can show what the change in metabolic rate is that allows them to eat pigstyle and lose wt.

I'd sure like to see that.

And please refute the study on the mice where the RESEARCHERS stated the mice had insulin resistant fat cells and metabolism of glucose in muscle didn't change.

Please show your studies.

 

[Animalkits]

And the crux of their argument is that you can take ALA and still eat sugar above and beyond what your muscle needs and you won't get fat because insulin is suppressed. Let's get real here.

 

[macro]

They also claim that only 20% of glycogen stores is muscle.



100% minus 20% is 80%. Simply said, 80% of the glucose is going into fat as ALA has no preference for muscle over fat and fact is that FAT would greatly outcompete muscle at grabbing it at a 4 to 1 ratio.

'

you need to read the posts, this has already been addressed.

you have to know more about physiology than to make a stupid argument like that.

are you forgetting all the other tissues of the boy that store glycogen, including the liver?

all body tissues store glycogen, it is just most prevalent in the liver (20% by weight) and muscle (1-2% by weight).

the only person that has mentioned "shoving glucose into fat" is YOU. and that is WRONG.

unless you are eating over 500grams of carbs a day, thats for a person with a normal mass, fat uptake of glucose is a NON ISSUE.


the main issue with carbs is not that they are stored as fat, but that they increase insulin release which increases uptake of fatty acids into fat as well as adipocyte differentiation. Once mature adipocytes become resistant to lipolysis (they excrete hormones like PGE2).


just because ALA and r-ala can IN ISOLATED MOUSE FAT CELLS, cause uptake does not mean that it does in a HUMAN system.

3T3-LT cells are mouse FAT CELLS that are MUCH MORE effective at glucose uptake than Human fat cells

 

[macro]

And the crux of their argument is that you can take ALA and still eat sugar above and beyond what your muscle needs and you won't get fat because insulin is suppressed. Let's get real here.

thats actually somewhat accurate. Though not in the way that you have worded it.

the lowering of plasma insulin has numerous benefits one of which is it results in, as compared to system with "normal" insulin production, elevated metabolism. Through improved GH action (lessened insulin inhibition), increased carbohydrate oxidation, as well as through PPAR-y related effects.

and once again you muscle in NOT the only tissue that stores glycogen.


also you will see greater glycogen uptake with meals that occur not after exercise. (here the benefit will be less (at least in muscle), particularly for endurance atheletes)