IGF mechanism shows you do want glucose resistance.

[Animalkits]

IGF mechanism shows you do want insulin resistance.

To much advertising on another group of threads diluting the message that you don't want glucose going into your fat cells. IGF works in such a way. That's exactly how it works.

These results indicate that the effect of IGF-I on lipogenesis in adipose tissue is not direct but via decreased serum insulin levels, which reduce the capacity of adipocytes to metabolize glucose.[b/]


IGF works by reducing insulin levels which reduces fat cells ability to take in glucose.
Hmm, I think that's resistance? Anyhow, it works by keeping glucose OUT of the fat cell!

Now why would I want to take something which puts glucose INTO the fat cell with or without insulin? IGF keeps it out and that's the king and that's good enough for me.

No glucose in my fat cells, please!

In the soleus muscle, the glycogen content and insulin-stimulated glucose incorporation into glycogen were increased in IGF-I-treated rats. In summary, IGF-I has opposite effects on glucose uptake in adipose tissue and skeletal muscle, findings which at least partly explain previous reports of reduced body fat mass, increased body cell mass, and increased insulin responsiveness after IGF-I treatment.

 

[macro]

Re: IGF mechanism shows you do want insulin resistance.

These results indicate that the effect of IGF-I on lipogenesis in adipose tissue is not direct but via decreased serum insulin levels, .[b/]


.

that is also how r-ala works, by reducing plasma insulin and increasing insulin sensitivity.

the problem is that you are looking solely at effects on isolated cell lines, in a system (a person) r-ala promotes muscle uptake of glycogen, reduces serum insulin and promotes fat loss (through both insulin reduction and MaPK as well as PPAR-y effects.

 

[macro]

btw- the title of your thread is dead wrong.

IGF-1 promotes insulin sensitivity and its actions are through reduction of plasma insulin. the exact same effects, with respect to serum insulin, that have been shown with R+ lipoic

 

[Animalkits]

Damn, it should be glucose resistance. Oh well.

Ok, but IGF is keeping glucose out while ALA is letting it IN even with lower insulin with the BONUS being that there is less insulin inhibition of lipase.

Again, I don't have a problem with lower insulin and blah, blah, blah, but with glucose still getting where I don't want itl

 

[macro]

Damn, it should be glucose resistance. Oh well.

Ok, but IGF is keeping glucose out while ALA is letting it IN even with lower insulin with the BONUS being that there is less insulin inhibition of lipase.

Again, I don't have a problem with lower insulin and blah, blah, blah, but with glucose still getting where I don't want itl

in isolated cells fat cell lines yes you get uptake, though with its MaPK effects on ppar-y antagonism on cellular differentiation, you get no new fat cells.

This uptake is not the case in a system (person)


btw- Insulin and igf-1 effects on pre-adipocytes= proliferation.
so taking these two together,exogenous, is probably not a good idea.


these are really the lesser factors, lowering of plasma insulin and increased overall insulin sensitivity... ARE.

 

[Animalkits]

However, insulin resistance in fat didn't change overall glucose metabolism

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.

 

[macro]

those are genetically engineered mice. and body fat was a very small portion of mass, wherein resistance would not have impact.

essentially they have altered the system and this adaptation occured, you really cant translate the results to mice, let alone humans.

its an interesting study, though have read it before.

 

[Drveejay11]

Hmmmmm.....WHO wants to delve into THIS relevant topic:

-HGH makes you insulin resistant yet IGF-1 increases insulin sensitivity (yet HGH--------->IGF-1).
-If IGF-1 renders you more slin-sensitive; then WHY is fatigue/lethargy experienced opposed to HGH not having these effects.
-Elaborate on the mechanisms and pathways involved with HGH fat loss and how this is feasible in an insulin-resitant environment

-Thanks

 

[Animalkits]

That is answered on my board under this sticky!

And why you take HGH with something that raises insulin a bit as well as with protein. Of course you could take insulin with HGH and this would be the reason why, that is if you aren't eating with it yet still want to increase pro syn. Take the H with food that has raised insulin. Therefore, if you were told to take H before bed or as soon as you wake up and didn't take in protein and some insulin response, you were wasting your money!

Somatostatin prevents the leucine-induced changes in plasma insulin and protein synthesis. However, somatostatin does not prevent leucine-induced changes in eIF4E binding to 4E-BP1 or eIF4G, suggesting that such changes are not sufficient by themselves to stimulate protein synthesis. Moreover, somatostatin attenuates the leucine-induced hyperphosphorylation of 4E-BP1 and S6K1 and completely prevents changes in phosphorylation of S6. Overall, the results of this study agree with those of Grizard and co-workers (8, 67) and suggest that the feeding- and leucine-induced increases in muscle protein synthesis above fasting values require an increase in the plasma insulin concentration.



Nevertheless, HGH goes into cells WITHOUT being converted to IGF. Right in the PDR it says HGH INCREASES insulin secretion. There is NOT enough IGF conversion to lower insulin and increase sensitivity OVER the increased insulin secretion. HGH causes insulin resistance by increased secretion of insulin even when cells are full of glycogen.

Would ALA mitigate this insulin problem by clearing insulin remains to be seen.

 

[Animalkits]

those are genetically engineered mice. and body fat was a very small portion of mass, wherein resistance would not have impact.

essentially they have altered the system and this adaptation occured, you really cant translate the results to mice, let alone humans.

its an interesting study, though have read it before.

Yes they are genetically engineered to be insulin resistant on fat cells demonstrating there is not some catastrophic event from insulin resistant fat cells which I addressed elsewhere/before.

They just change one aspect of the system where diabetes and obesity changes many, therefore, 'you really can't translate the results to normal humans.'

 

[DrJMW]

HGH-induced insulin resistence is slight and mild. HGH-induced hypothyroidism is much more apparent. Overcoming the slight insulin resistence is easy: high protein, moderate clean carb, low clean fat diet. It works every time. I am assuming that the HGH user is keeping his dosing between 2-4IU daily.

 

[macro]

Yes they are genetically engineered to be insulin resistant on fat cells demonstrating there is not some catastrophic event from insulin resistant fat cells which I addressed elsewhere/before.

They just change one aspect of the system where diabetes and obesity changes many, therefore, 'you really can't translate the results to normal humans.'

they are not "insulin resistant" ... they have no insulin receptor in fat tissue. Its not the same thing. and this condition exists from birth so through the grwoth cycle there are adaptations. This will not work for you.

 

[moresize2]

i'm using r-ala right now and with the same cal,carb,protein intake i'm getting leaner?


i'm not getting fat


just giving feed back

 

[Drveejay11]

-Elaborate on the mechanisms and pathways involved with HGH fat loss and how this is feasible in an insulin-resitant environment

 

[Drveejay11]

That is answered on my board under this sticky!

Damn it.....check your PM's. I am having prob's with your site. Thanks

 

[Ken]

Damn nice read fellas.. Keep the constructive comments comin.. Good to see some knowledgable peeps getting along and talking things over..

 

[Animalkits]

You know, macro needs to put this in layman's terms so people like Tx can understand.

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.

As for the HGH, HGH upregulates T3 so you are not hypo, but hyper at least for the first month or so.

This is well proven and research has even been done comparing HGH against T3 with IGF to see if the results were the same.

 

[ulter]

i'm using r-ala right now and with the same cal,carb,protein intake i'm getting leaner?


i'm not getting fat


just giving feed back

You don't get fat from using R+ Lipoic acid. Virtually no one has but don't think that fact is going to stop Animal from trying to tell you it does. In nearly 2 years on the market not a single user has ever reported fat gains from Glucorell R. That's what makes this whole argument so silly to me. 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.


Animal, get real bro. You want to take study done with mice that have been genetically engineered and apply it to humans. And then you call Macro the jackass.

 

[Animalkits]

Show your study that the researcher is wrong and have them change the wording in their peer reviewed publication.

I'm sure leptotrim has the same claims of everyone being satisfied, too.

Interesting that you choose to avoid the posts on these very threads where people say they quit taking it as it wasn't doing them any good.

Oh, I know, I planted those.

We are waiting for the studies to show us wrong and I am NOT the only one. Many are having problem with sugar going into fat cells.

 

[Animalkits]

Virtually no one has but don't think that fact is going to stop .

CAN ANYBODY ELSE READ THAT STATEMENT?

Virtually noone. HAHA!