IGF mechanism shows you do want glucose resistance.

Animal, you haven't posted any studies done with R+ Lipoic Acid. You keep posting Dr Packer's study done with racemic ALA.

This is what you posted as proof that R+ Lipoic Acid makes you fatter on you first thread. This study uses ALA.

Lipoic Acid Inhibits Adipocyte Differentiation by Regulating Pro-adipogenic Transcription Factors via Mitogen-activated Protein Kinase Pathways*
Kyung-Joo Cho , Hae-Eun Moon , Hadi Moini , Lester Packer , Do-Young Yoon ¶ and An-Sik Chung


Dr Packer doesn't believe that racemic ALA should be used for therapeutic applications, which this would be, he says to use R+ ALA instead.

"R[+]-LA [that is, R(+)-lipoic acid], and not a racemic mixture of R[+]-and S[-]- LA, should be considered a choice for therapeutic applications."
Dr. Lester Packer and colleagues, in Free Radical Biology and Medicine.

So if the author of the study you posted says not to use racemic ALA. What's your point? There is no racemic ALA in Glucorell R.

Dr Streeper from the U of Arizona proved that glucose uptake enhancement with ALA is stereospecific. That the pure R+ is what should be used.

"We have presented in this study new information indicating that this enhancement of glucose metabolism is sterospecific, with the R(+)-enantiomer being much more effective than the S(-)- enantiomer."
Dr. Ryan Streeper and colleagues, in The American Journal of Physiology.


So what is your point? Ok we won't use ALA which is what we told you not do since you put it in your anarchy stack 2 years ago. But you've left it in there anyways.
 
Animalkits said:
You know, macro needs to stop being a jackass and stop making up bullshit.

This quote is right from the study and he sits there and makes it into something else to suit himself.

'Although FIRKO mice show insulin resistance in the adipose tissue, whole-body glucose metabolism is not affected.'

I didn't write the study and I didn't write the conclusion. You just wanna start bullshit.

Again, HE made it about ME!

you are the jackass. the study says no such thing.

DO YOU KNOW WHY?

BECAUSE THEY HAVE NO INSULIN RECEPTOR IN THEIR ADIPOSE TISSUE.

what you have done, foolishly is taken that quote from someone else writing about the study.

those cells are not insulin resistant, they are insulin IMMUNE. and they were born that way.
 
Last edited:
from another study on FIRKO mice

Indeed, the phenotype of aging FIRKO mice shows similarities with the phenotype of food-restricted mice, such as reduced adiposity, trend to lower insulin levels, and protection from decreased insulin sensitivity
Extended Longevity in Mice
Lacking the Insulin Receptor in
Adipose Tissue
Matthias Bluher, Barbara B. Kahn, C. Ronald Kahn


interestingly enough these are the same effects that r-ala has shown in that model.

Streeper RS, Henriksen EJ, et al, Tritschler HJ. Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol 1997 Jul; 273(1 Pt 1): E185-91

Hagen et al, "(R)-alpha-Lipoic acid-supplemented Old Rats Have Improved Mitochondrial Function, Decreased Oxidative Damage, and Increased Metabolic Rate," FASEB J 1999 13:411-418

Freisleben HJ, Neeb A, Lehr F, Ackermann H. Influence of selegiline and lipoic acid on the life expectancy of immunosuppressed mice Arzneimittelforschung 1997 Jun; 47(6): 776-80
 
ronmolina said:
I think I have seen this debate before.

how about this one :)

Horm Metab Res. 2001 Mar;33(3):156-62.


Recombinant human growth hormone, but not insulin-like growth factor-I, enhances central fat loss in postmenopausal women undergoing a diet and exercise program.

Taaffe DR, Thompson JL, Butterfield GE, Hoffman AR, Marcus R.

Epidemiology, Demography, and Biometry Program, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA. dtaaffe@hms.uq.edu.au

We examined the effect of recombinant human growth hormone (rhGH) and/or recombinant human insulin-like growth factor-I (rhIGF-l) on regional fat loss in postmenopausal women undergoing a weight loss regimen of diet plus exercise. Twenty-seven women aged 59-79 years, 20-40% above ideal body weight, completed a 12-week program consisting of resistance training 2 days/week and walking 3 days/week, while consuming a diet that was 500 kcal/day less than that required for weight maintenance. Participants were randomly assigned in a double-blind fashion to receive rhGH (0.025 mg/kg BW/day; n = 7), rhIGF-I (0.015 mg/kg BW/day; n = 7), rhGH + rhIGF-I (n = 6), or placebo (PL; n = 7). Regional and whole body fat mass were determined by dual X-ray absorptiometry. Body fat distribution was assessed by the ratios of trunk fat-to-limb fat (TrF/LimbF) and trunk fat-to-total fat (TrF/TotF). Limb and trunk fat decreased in all groups (p < 0.01). For both ratios of fat distribution, the rhGH treated group experienced an enhanced loss of truncal compared to peripheral fat (p < 0.01), with no significant change for those administered rhIGF-I or PL. There was no association between change in fat distribution and indices of cardiovascular disease risk as determined by serum lipidilipoprotein levels and maximal aerobic capacity. These results suggest that administration of rhGH facilitates a decrease in central compared to peripheral fat in older women undertaking a weight loss program that combines exercise and moderate caloric restriction, although no beneficial effects are conferred to lipid/lipoprotein profiles. Further, the effect of rhGH is not enhanced by combining rhGH with rhIGF-I administration. In addition, rhIGF-I does not augment the loss of trunk fat when administered alone.
 
If you wanna discuss like normal humans, fine, but unless we hear from the researchers that they meant something else which isn't likely to happen, I think this is pretty plain english.

'Although FIRKO mice show insulin resistance in the adipose tissue, whole-body glucose metabolism is not affected.

It's their words.
 
ulter said:
But we meet any challenge to the science behind it so here we are, during the busiest time of the year, spending hours trying to get one lonely soul to understand he has it wrong.


And we appreciate it. I might only speak for myself, but in the last week, I've learned more about ala, r-ala, insulin, lipolysis, and lipogenises than I have in 5 years.

Thank you, and that goes to macro and animal as well. I am amazed and somewhat intimidated by you guys and your knowledge of biochem and it's pertinence to us as bb'ers.
 
Even through all the bitchin' I did learn more than I had known, well to be more exact, I now know all the reasons presented are thoroughly and completely backed up the the research as well as the mechanisms I presented.

You might want to look at the all the 'stupid, idiot, fool, uneducated, etc in their posts and let's not forget who was posting pictures and personal information out.

Anyhow, I've gotten out all the info and exposed this for what it is and you can now do what you want with the info. You wanna believe studies on diabetics, obese, and post menopausal women, it's your $ lost. I'm done.
 
"Insulin and igf-1 effects on pre-adipocytes= proliferation.
so taking these two together,exogenous, is probably not a good idea
."




I am a type 1 diabetic, so I take nolvalog everytime I eat. Generally totaling 40 units per day, and lantus which is long acting 30 units a day....

anyways I just got some igf lr3, but this comment confused me...Could you give me some info?

I would really appreciate it
 
"Insulin and igf-1 effects on pre-adipocytes= proliferation.
so taking these two together,exogenous, is probably not a good idea
."




I am a type 1 diabetic, so I take nolvalog everytime I eat. Generally totaling 40 units per day, and lantus which is long acting 30 units a day....

anyways I just got some igf lr3, but this comment confused me...Could you give me some info?

I would really appreciate it

7 yr old thread bro....
 
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