r-ALA can make you FATTER!

[Animalkits]

OH wait, I see, so now we never need insulin, right?

 

[nuttz565]

Man it almost seems not to be worth taking r-ala, I had ordered some but now I see so many posts with conflicting messages about it I almost don't even know if it is worth spending money on...........

 

[Animalkits]

Now I wonder what happens to that glucose which IS NOT converted to glycogen.

And I'm sorry to say that Mr Wonderful still just DOES NOT GET THE FACT THAT I NOR ANYBODY ELSE WANT GLUCOSE BEING JAMMED INTO OUR FAT CELLS.

And I don't want glycogen synthesis inhibited when I'm trying to recover. Sorry if YOU think we are all diabetics and obese and want a glucose disposal agent, but we are genetically and biochemically different than those people and we DO NOT want the ALA to do the same for us as them!

All those in said groups who have used glucose disposal agents of any kind are now lean and mean, right?



Alpha-lipoic acid inhibits glycogen synthesis in rat soleus muscle via its oxidative activity and the uncoupling of mitochondria.

Dicter N, Madar Z, Tirosh O.

Institute of Biochemistry, Food Science and Nutrition, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel.

alpha-Lipoic acid (LA) is currently being investigated as a glucose-lowering agent for diabetes control; it is also considered a powerful dietary antioxidant. The objective of this study was to investigate the fate of glucose in isolated rat muscles incubated with LA and determine its effects on intramuscular redox status. Rat soleus muscles were incubated for up to 60 min with 2.4 mmol/L LA in the presence or absence of insulin. Intramuscular concentrations of LA were evaluated (uptake and reduction), and glycogen synthesis, glucose oxidation, intramuscular reactive oxygen species (ROS) production and mitochondrial membrane potential investigated. Insulin enhanced glycogen synthesis, whereas LA decreased rates by >50%. LA elevated ROS production and in combination with t-butylhydroperoxide, an oxidant, additively inhibited glycogen synthesis rates by 80%. Insulin acted as an antioxidant and attenuated ROS production by 30%. LA uncoupled the mitochondria and accelerated glucose oxidation 1.5-fold relative to the control. The glycogen synthesis pathway was found to be dependent on mitochondrial function because treatment with mitochondrial inhibitors eliminated the majority of glycogen synthesis. These data show that in this model, LA acts as a mild prooxidant, causing mitochondrial uncoupling and inhibition of glycogen synthesis. It appears that LA regulates glucose metabolism in the muscle differently than insulin.

 

[Animalkits]

Man it almost seems not to be worth taking r-ala, I had ordered some but now I see so many posts with conflicting messages about it I almost don't even know if it is worth spending money on...........

"Ahh, and my quest is being satisfied because you and others are being sold a bill of goods because the reason to take ALA is NOT as a glucose disposal agent, but as a mitochondrial anti-oxidant with ALC and ALA stimulates glutathione.

THAT it what it was first used for and now they are jumping on the quick fix market and applying diabetic and obese principals on the general population, athlete. WRONG!

 

[Animalkits]

100mg ylds 260um, but that's just conveniently just over the cusp, isn't it?

' ' In our study, LA at lower concentrations (100 µM) promoted adipogenesis whereas at higher concentrations (250 and 500 µM)it was inhibitory''

Nobody tells you how long the rise is or how long the peak is or how long the fall is.

 

[Animalkits]

Also for those of us who are so ignorant and unworthy, it should be known that insulin INHIBITS lipolysis which is entirely different from promotion of lipogenesis.


Just another bullshit batch of word twisting they are using to misconstrue the true definition.

And I guess glucose into the fat cells is magically being made into protein?

 

[macro]

Also for those of us who are so ignorant and unworthy, it should be known that insulin INHIBITS lipolysis which is entirely different from promotion of lipogenesis.


Just another bullshit batch of word twisting they are using to misconstrue the true definition.

And I guess glucose into the fat cells is magically being made into protein?

you are really dumb.

the purpose of thermorexin a "fat burner" is to enhance lipolysis.

If you had actually read the post, and understood it, you would see that they are not mutually exclusive.

basically in a hypocaloric environment, adipogenesis is a relative non-issue- inhibition of lipolysis is.

and btw- since the whetting stone has not been in use lately..... insulin also promotes adipogenesis.


and before you try to argue the insulin/amino connection.... where you were pleading for help on a board that you deride...

lets nip that in the bud...

J Appl Physiol 2002 Sep;93(3):1168-80 Related Articles, Links


Invited Review: Role of insulin in translational control of protein synthesis in skeletal muscle by amino acids or exercise.

Kimball SR, Farrell PA, Jefferson LS.

Department of Cellular and Molecular Physiology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA

Protein synthesis in skeletal muscle is modulated in response to a variety of stimuli. Two stimuli receiving a great deal of recent attention are increased amino acid availability and exercise. Both of these effectors stimulate protein synthesis in part through activation of translation initiation. However, the full response of translation initiation and protein synthesis to either effector is not observed in the absence of a minimal concentration of insulin. The combination of insulin and either increased amino acid availability or endurance exercise stimulates translation initiation and protein synthesis in part through activation of the ribosomal protein S6 protein kinase S6K1 as well as through enhanced association of eukaryotic initiation factor eIF4G with eIF4E, an event that promotes binding of mRNA to the ribosome. In contrast, insulin in combination with resistance exercise stimulates translation initiation and protein synthesis through enhanced activity of a guanine nucleotide exchange protein referred to as eIF2B. In both cases, the amount of insulin required for the effects is low, and a concentration of the hormone that approximates that observed in fasting animals is sufficient for maximal stimulation. This review summarizes the results of a number of recent studies that have helped to establish our present understanding of the interactions of insulin, amino acids, and exercise in the regulation of protein synthesis in skeletal muscle.

 

[macro]

Now I wonder what happens to that glucose which IS NOT converted to glycogen.

And I'm sorry to say that Mr Wonderful still just DOES NOT GET THE FACT THAT I NOR ANYBODY ELSE WANT GLUCOSE BEING JAMMED INTO OUR FAT CELLS.

And I don't want glycogen synthesis inhibited when I'm trying to recover. Sorry if YOU think we are all diabetics and obese and want a glucose disposal agent, but we are genetically and biochemically different than those people and we DO NOT want the ALA to do the same for us as them!

All those in said groups who have used glucose disposal agents of any kind are now lean and mean, right?



Alpha-lipoic acid inhibits glycogen synthesis in rat soleus muscle via its oxidative activity and the uncoupling of mitochondria.

Dicter N, Madar Z, Tirosh O.

Institute of Biochemistry, Food Science and Nutrition, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel.

alpha-Lipoic acid (LA) is currently being investigated as a glucose-lowering agent for diabetes control; it is also considered a powerful dietary antioxidant. The objective of this study was to investigate the fate of glucose in isolated rat muscles incubated with LA and determine its effects on intramuscular redox status. Rat soleus muscles were incubated for up to 60 min with 2.4 mmol/L LA in the presence or absence of insulin. Intramuscular concentrations of LA were evaluated (uptake and reduction), and glycogen synthesis, glucose oxidation, intramuscular reactive oxygen species (ROS) production and mitochondrial membrane potential investigated. Insulin enhanced glycogen synthesis, whereas LA decreased rates by >50%. LA elevated ROS production and in combination with t-butylhydroperoxide, an oxidant, additively inhibited glycogen synthesis rates by 80%. Insulin acted as an antioxidant and attenuated ROS production by 30%. LA uncoupled the mitochondria and accelerated glucose oxidation 1.5-fold relative to the control. The glycogen synthesis pathway was found to be dependent on mitochondrial function because treatment with mitochondrial inhibitors eliminated the majority of glycogen synthesis. These data show that in this model, LA acts as a mild prooxidant, causing mitochondrial uncoupling and inhibition of glycogen synthesis. It appears that LA regulates glucose metabolism in the muscle differently than insulin.

1. this study used racemate
2. this study used MILLIMOLES not MICROMOLES
3. its an isolated system
4. Its well known that anti-oxidents work as pro-oxidents at high dosages

 

[macro]

btw- its hilarious to see you attacking r-ala when you tout ALA as part of your "anarchy stack".

 

[ulter]

Animal why are you so dead set on showing your ignorance on this subject. You used to be smart enough to stay out of arguments that you had no knowledge of. And here you are now arguing a subject that you don't understand and have spent little or no time researching, with a man who holds 3 degrees, one a PhD, and who has spent most of the last year pouring over every word of literature ever written on this subject.

You should get on that bicycle you ride and take on Lance Armstrong in the next Tour de France, you've got a much better chance there.

 

[moresize2]

bump

 

[Animalkits]

Thanks for the board of ignorance showing up in full force tonight.

Anybody noticing how they use studies to their favor in one argument and then change it to use it another way in another argument?

Admongers, when in the hell are you gonna tell people why it's so good to have glucose jammed into your fat cells and how it's so good? I want to know why I workout out to improve muscle sensitivity and decrease fat cell sensitivity to have it ruined by ALA.

C'mon we all want to hear it.

ALA also makes you hungry, now why is that? C'mon!

It's obvious YOU don't know what the anarchy stack is nor do you know what ALA was originally used for and what it's only true use is which IS NOT a glucose disposal agent.

When are you gonna tell all the people that all your sacred studies are on obese and diabetics who have different genetics and physiology?

Maybe when you post up all their before and after pictures and how ALA solved all their problems?

Because somebody has a degree in shit, we should buy it and eat it cause he gets paid to sell it. Funny, you nor mr smarto can prove what it does in normal humans.

Right, I only gradeeated the 3rd grade, but it sure is easy to expose a scam and all your little stories aren't convincing anybody of anything! Hilarious that other threads about problems were out there, but now the goons are over here?

And that's a good red herring that nobody should talk about a subject but YOU! The church and the nazi's thought that way, too!


Take on Lance? Ha! At least I'm still an athlete and not a fat ass behind a desk looking to scam people for a buck.

I'll just have lance get on the track one day cause I know it will make some no mind happy. Whatever that has to do with anything in this thread is mystical. Maybe ALA works for Lance?

I'll sleep well though I'm sure the unscrupulous will too!

Roughly 40% of studies are inconclusive of insulin promoting protein synthesis. I'm sure you read the entire thing and see that absence of insulin and minimal insulin are entirely different! But I'm sure you will present some study to show that you can eat and not produce insulin.

Keep tripping over yourselves.

 

[Animalkits]

And where is the same study with r-ALA showing it to be different? Hmmm.

 

[Animalkits]

It's also obvious that you two know absolutely nothing about chemical use in elite level sports, but I'm sure you'll tell the world of elite athletes why you DO NOT ever need any insulin above fasting to improve their recovery.

At least you guys are good for a laugh.

 

[Animalkits]

And just so you don't miss it and everyone can get the answer,

Why do they want glucose indiscriminately jammed into their fat cells?

 

[macro]

when you read the studies and are able to understand them, come back and play.

the answer to your last simple question has been answered several times..... r-lipoic inhibits adipogenesis

no one has suggested that the dosage amount in thermorexin is sufficient for this effect, but as has also been noted... thermorexin is intended to be used in a hypocaloric environment.. where adipogenesis is not an issue.

as has already been pointed out to you several times, the lowering of plasma insulin aids in lipolysis as well as inhibiting adipogenesis.

 

[Animalkits]

In the obese and diabetics. Try again!

However, these studies do not reveal the contributory role of insulin in the feeding-induced responses because, in both animal models, plasma concentrations of the hormone are elevated in fasted compared with control animals, and, in ob/ob mice, plasma insulin concentrations are increased by feeding.

And you are a liar. It inhibits adipogenesis in pre-adipocytes. Nice try.

Why is it good to have more glucose in my fat cells? You seem to have a real aversion to answering this, don't you?

 

[macro]

no aversion. the question is without merit as that is not the case.

its quite odd that you ignore the fact that people that use both ALA and R-ala (atheletes and bodybuilders) all report leaning effects.

and calling anyone a liar is foolish, when you fail to even grasp a basic understanding of the systems involved. Hence are unable to distinguish between truth and falsehood. Though in this case there exists neither, only scientific findings and theoretical models.

 

[Animalkits]

Well that exactly makes you a liar because EVERYBODY knows damn well that ALA of any kind disposes glucose into muscle AND FAT CELLS! You try and spew some tripe that there is some 'competition' for the glucose, but that's just more crap.

So you still CANNOT answer the question, but I'm the one with no knowledge of the subject? HA! You don't even have rudimentary knowledge of the most basic mechanisms about which you quack.

Wait, I know, I just didn't see it. I have to eat more like a pig with more glucose so I can spend more money and buy more pills to dispose of the glucose so that I won't get fat.

ARe you that ridiculous? I'm eating to much of a substance (glucose) which isn't improving my protein synthesis so now I have to take something to get rid of it? That's your best case just for the argument of not answering what happens to the glucose going into fat cells via r-ala!

The best you got is you can spend more money to eat more of a useless energy source? Eat more sugar and take my pill to get rid of it!

AAHHAHAHAHAHAHAHAAAAAAAAAAAAAA!


Oh shit! I guess I am the stupid one and uneducated cause I'm not in on this scam or maybe it's that I have ethics.

 

[macro]

maybe it's that I have ethics.

its well known that is not the case