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napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
RESEARCHSARMSUGFREAKeudomestic
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsRESEARCHSARMSUGFREAKeudomestic

one thing i;ve always wondered about ALA...

i had thought about looking at the NIDDM medications as a reference point, but i have had 'teaching' in this area and it has never been mentioned as a side effect of them, and i;ve also not seen it mentioned in any pharmacology texts that i've read.

my pubmed searches have been fruitless as well, but i hate that damned thing anyway as i can never find what i want, so it left me wondering about ALA specifically

you turned up anything on the research front? you seem quite good at finding the net sources of info...and thanx for the bump
 
danielson said:
by what mechanism? im unsure how it can as i;ve never seen biotin mentoned as an essential co-enzyme for insulins actions

i believe biotin is an essential cofactor for lipoamide (ala in its amide form) during the pyruvate dehydrogenase step preceeding the creb's cycle. it's been a little while since i took biochem so i could be off. but i think i'm right.

and i've never heard biotin being required to mediate any of ala's actions in increasing insulin sensitivity.

it's more of ala depleting the body's store of biotin that is the reason you're supposed to take the 2 together.
 
i just talked to an endocrinologist on another board and he says that something like ALA will be better than using nothing for those at risk of type 2 diabetes. He also said that yes, the islet of langerhan cells will have a negative feedback loop which decreases insulin production but that that is a good thing as they will not have to work as hard to produce as much insulin and will therefore last longer. I am not sure where he stands on the risks of long term atrophy of Islet of Langerhan cells but i am trying to clarify that. He says the answer is too complex and he doesnt have time to explain it but that the risk of contracting type II diabetes is going to be lower on ALA.
 
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hmm

makes sense.....im not sure whether your beta-cell number wont decrease on the basis of something that improves the effects/actions of insulin

this is probbly enough for me, if i manage to corner an endocrinologist or pharmacologist i'll ask them, however the last one i asked had never heard of ALA (was also a diabetologist) and labelled it a 'homeopathic' herb or something similar :rolleyes:
 
bump.. Very interesting. I'm taking GlucorellR in large doses for 4 months straight. Was wondering the same effect. Also, if there's a crash after stopping using it.
 
This could be an interesting debate. However, I question the relevance of your inquiry to r-ALA. Are you worried about pancreas atrophy? You draw a parallel between adrenal gland and pancreas, yet the atrophy of adrenal gland results from exogenous administration of glucocorticoids. ALA is not insulin, insulin activates a pathway through which GLUT-4 is translocated from the intracellular compartment into the membrane, thus the cell surface becomes receptive to insuling and glucose uptake which results in synthesis of a few kinases which are responsible for translocation of GLUT-4 onto the membrane and glycogen synthesis. ALA acts in a few ways:
1) it increases insulin stimulating effects on the pathway to GLUT-4 translocation
2) increase the expression of GLUT-4 transporters in the membrane - larger surface=more uptake
3) ALA has anti-oxidative effects on free radicals (perroxides/reactive oxygen species) which even in small amounts can totally inhibit GLUT-4 expression and kinases responsible for glycogen synthesis (welcome diabetis)

Therefore ALA's action in the body is merely of a facilitator to insulin and glucose clearance, but i'm yet to see anything to mention that it reduces the serum/secretion of insulin. I think the confusion about ALA and pancreatic atrophy stems from a myth that ALA is an insuin mimic - but it is not.
 
yeah its why we had the confusion juve, when talking about it to my friends we realised the negative feedback in regards to the corticosteroids were due to the fact that exogenous steroid was being administered, we were unsure about the effects of something that increases/facilitates the action of insulin would have on the pancreas.
 
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