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Bodybuilding Peptides and Insulin Learn and discuss the different aspects of peptide cycles, doses, how to mix HGH, IGF-1, MGF, Insulin as well as many other Anabolic Peptides


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  #1  
Old 04-18-2011, 11:48 PM
Goldenchook Goldenchook Is Off Line
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Aod9604

I was wondering whether the peptide AOD-9604 is of any interest to body builders?

I understand the peptide has been shown to produce lipolysis or the breakdown of fetty cells.

The peptide was shown to be ineffective orally, however the company that "owns" the peptide has teamed up with a dermal delivery company to produce a topical application to deliver AOD-9604 to a localised area of fat, called body shaper.

This product has been approved for release as an OTC cream and is set for global release in Australia by end of April, followed by USA, Europe, India and SE Asia.

Does anyone think it could be a relevant product for body builders?

I appreciate anyone's feedback and thanks in advance.
  #2  
Old 04-19-2011, 12:13 AM
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I would say yes..

while this study was on mice.. it does sound promising (given that I spent about 4 minutes search and reading this one article.. I would have to research more.. But yes!!




The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta(3)-AR knock-out mice.
Abstract
Both human GH (hGH) and a lipolytic fragment (AOD9604) synthesized from its C-terminus are capable of inducing weight loss and increasing lipolytic sensitivity following long-term treatment in mice. One mechanism by which this may occur is through an interaction with the beta-adrenergic pathway, particularly with the beta(3)-adrenergic receptors (beta(3)-AR). Here we describe how hGH and AOD9604 can reduce body weight and body fat in obese mice following 14 d of chronic ip administration. These results correlate with increases in the level of expression of beta(3)-AR RNA, the major lipolytic receptor found in fat cells. Importantly, both hGH and AOD9604 are capable of increasing the repressed levels of beta(3)-AR RNA in obese mice to levels comparable with those in lean mice. The importance of beta(3)-AR was verified when long-term treatment with hGH and AOD9604 in beta(3)-AR knock-out mice failed to produce the change in body weight and increase in lipolysis that was observed in wild-type control mice. However, in an acute experiment, AOD9604 was capable of increasing energy expenditure and fat oxidation in the beta(3)-AR knock-out mice. In conclusion, this study demonstrates that the lipolytic actions of both hGH and AOD9604 are not mediated directly through the beta(3)-AR although both compounds increase beta(3)-AR expression, which may subsequently contribute to enhanced lipolytic sensitivity.

Heffernan M, Summers RJ, Thorburn A, Ogru E, Gianello R, Jiang WJ, Ng FM.

Department of Biochemistry and Molecular Biology, Monash University, Clayton, Australia 3800.
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  #3  
Old 04-19-2011, 12:22 AM
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The Effects of Human GH and Its Lipolytic Fragment (AOD9604) on Lipid Metabolism Following Chronic Treatment in Obese Mice and ß3-AR Knock-Out Mice

It is well established that hGH is a lipolytic hormone (15), but the exact mechanisms used are still unclear. In this paper we present data that suggest that hGH and its lipolytic fragment (AOD9604) induce their chronic in vivo actions on lipolysis in part by modulating the expression of the ß3-AR. Human GH has been shown to affect the in vivo expression and function of ß-ARs in vivo in sheep (16). Data presented in this paper indicate that chronic administration of hGH influences expression of the ß3-AR in adipose tissue in the ob/ob mouse. In brown adipose tissue (BAT), these compounds also increase expression of ß3-AR expression in the lean C57BL/6J mouse. The increase in expression induced by chronic hGH or AOD9604 treatment correlated with the decrease in adipose tissue mass. We therefore hypothesize that treatment with either hGH or AOD9604 enhances ß3-AR expression, which has been observed in murine 3T3-F442A and human SK-N-MC cells in vitro (11).
Both AOD9604 and, to a greater extent, hGH increase body weight in lean mice, compared with saline-treated animals. This is in the absence of an increase in fat mass, which suggests an increase in lean body mass occurs with these compounds. This supports previous work with hGH in rodents and humans (17). Both compounds have also been previously shown to reduce body weight and adiposity in obese mice (11). The effects of hGH and AOD9604 occur without significant changes to caloric intake. It has been reported that hGH increases, reduces, or does not change food intake in which the differences are attributed to variations in hGH preparations, concentrations, and animals used between different laboratories.

The effects of hGH and AOD9604 on fat metabolism may be mediated by an alteration in the expression of a lipolytic/antilipogenic gene. The ß3-AR is a major lipolytic receptor identified in rodent fat cells (18) that mediates its effects through G protein coupling to adenylate cyclase, generation of cAMP, and stimulation of PKA (19). This enzyme then phosphorylates proteins in the lipolytic cascade, including hormone-sensitive lipase (20). In BAT, the ß3-AR stimulates uncoupling of the electron transport chain, enhancing the ability of mitochondria to generate heat in preference to ATP through the dissipation of the electron gradient (21). Mice that lack this receptor have lower rates of resting energy expenditure (0.0041 vs. 0.0047 kcal/min, P < 0.02) and lower rates of fat oxidation (0.00019 vs. 0.00030 g/min, P < 0.02) than control mice (data not shown).

AOD9604 and hGH appear to act in a similar manner to induce their effects on body weight regulation and adipose tissue mass in vivo. However, in vitro studies have demonstrated a number of differences suggesting that the two compounds operate via unique signaling pathways to control the regulation of the ß3-AR. These studies suggested that AOD9604 had no interaction with the ß3-AR or hGH receptors (11).

In lean animals, neither AOD9604 nor hGH had any effect on epididymal white adipose tissue mass or expression of ß3-AR RNA, indicating that in lean animals, this fat tissue is not a major target for these drugs in this study. In contrast, the mass of BAT in lean animals was reduced by both hGH and AOD9604, and ß3-AR RNA expression was increased by both these compounds. This could possibly suggest that the increased expression of ß3-ARs in brown adipocytes sensitizes catecholamines to dissipate heat.

In ob/ob mice, both AOD9604 and hGH reduced both white and brown adipose tissue mass and increased ß3-AR RNA expression. This suggested that an elevation in ß3-AR RNA expression is associated with increased fat metabolism and a reduction in the fat tissue mass in the ob/ob mouse model. Obese mice have lower levels of ß3-AR expression in their adipose tissues than lean mice, shown in this study and others (14). The ability of AOD9604 and hGH to increase the level of ß3-AR RNA expression in obese mice to a level that is comparable to those in lean mice is an exciting finding. However, it must also be considered that both hGH and AOD9604 may influence the expression of other members of the adrenergic pathway, such as the ß1-ARs, hormonesensitive lipase, and signaling proteins, which are all expressed in adipose tissue and associated with lipolysis. The importance of the change in ß3-AR expression with AOD9604 and hGH in humans is not established and will depend on the use of potent and selective ß3-AR agonists that are active at the human receptor.

From this study it appears that the ß3-AR is an important contributor to the effects observed on body weight in obese mice treated with AOD9604 and hGH. To determine whether the ß3-AR is partly responsible for this effect, we examined the effects of AOD9604 and hGH in the ß3-KO mouse. The ß3-KO mouse is not grossly obese, but female mice have increased fat depots (21) and the mice do develop late-onset obesity (Summers, R. J., personal communication). AOD9604 and hGH increased body mass and decreased BAT mass in the WT strain but had no effect in the KO animals. In WT mice, plasma glycerol was increased in response to AOD9604 and hGH treatment (4 wk). However, in the KO mice, only hGH resulted in increased levels of glycerol in the KO mice, and this effect was significantly less than that observed in the WT mice. This suggests that the regulation of the ß3-AR is essential in the ability of AOD9604 and hGH to mediate chronic effects on lipolysis and fat mass reduction.

The effect of AOD9604 and hGH on ß3-ARs in adipose tissue is believed to be a direct action of these compounds and not an effect secondary to the fat metabolism, given that both AOD9604 and hGH can influence ß3-AR expression and function in a nonadipocyte human cell line (11). Hence, the ß3-AR appears to be necessary for the chronic effectiveness of AOD9604 on lipolysis in BAT.

The acute effect of AOD9604 and BRL37344 (a ß3-AR agonist) on energy expenditure and substrate oxidation rates in WT and KO mice was also assessed. KO animals had lower energy expenditure, lower fat oxidation, and increased glucose oxidation, compared with the WT controls (data not shown). Injection of WT mice with a single dose of BRL37344 or AOD9604 increased energy expenditure and fat oxidation and decreased glucose oxidation. In the KO animals, BRL37344 failed to elicit any response in these metabolic parameters, clearly demonstrating that its effects are mediated exclusively through the ß3-AR. AOD9604 did elicit a response in the KO mice, increasing fat oxidation and energy expenditure, although the response was not as great as in WT mice, suggesting that ß3-ARs are not responsible for the acute biological response of AOD9604 on lipid metabolism. This is consistent with our previous findings in which AOD9604 was shown not to bind to the ß3-AR (11). The size and duration of the metabolic responses to AOD9604 in the ß3-AR KO animals was different from that observed in the control wild-type mice. The response was more rapid, shorter in duration, and greater in peak response. This may be because the KO animals are more acutely sensitive to lipolytic agents, a compensation for the ablation of the major lipolytic receptor.

These findings suggest that the acute effects of AOD9604 are quite different from the chronic effects. Enhanced ß3-AR expression appears to play a major role in the chronic effectiveness of the compound in terms of fat metabolism and weight loss. The acute effects observed in this study confirm that the ß3-AR is not the sole mediator of this action. The increase in ß3-AR expression in response to hGH and AOD9604 would permit enhanced lipolytic sensitivity. Identification of the components of the intracellular pathway(s) and effector(s) activated by AOD9604 are currently being investigated. The results presented in this paper suggest that the effectiveness of AOD9604 and hGH may partly rely on their ability to increase levels of ß3-AR RNA expression in models of obesity in which the numbers of the lipolytic receptor are low. These unique properties may give AOD9604 an advantage over other lipolytic agonists such as adrenergic agents and hGH, which exhibit undesirable side effects when administered chronically (22)
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  #4  
Old 04-19-2011, 12:54 AM
Goldenchook Goldenchook Is Off Line
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Thanks Basskiller.

I'm pretty sure that AOD has been cleared as safe for human consumption, and therefore studies with humans will have been done.

I know they are testing whether AOD can assist in decreasing osteoporosis, but the only test for fat reduction on humans failed because it couldn't bypass the gastro-intestinal system, hence the new mode of application through the skin.

I will try and find some relevant articles involving humans.
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Old 04-19-2011, 01:38 AM
Goldenchook Goldenchook Is Off Line
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Below is information about a study that showed oral aod was ineffective, and why the topical application may solve the problem.

Is AOD recognized at all in body building or is it seen as ineffective or not of enough effectiveness.

""AOD9604 failed as an anti-obesity drug. In a 536-patient Phase IIb randomised,
placebo-controlled trial of AOD9604, results of which were reported in February
2007, the drug:
• failed to achieve a statistically significant weight loss in any dosage group
after either 12 weeks or 24 weeks of treatment; and
• showed precious little overall weight loss - even after allowing for the formal
diet and exercise programme that had been put in place for this trial (and had
not been for previous trials) the weight-loss results were sparse, with less
than 1 kg drop across all dose groups6 at both measurement points.""


However,

AOD9604 did burn fat for at least one trial group. When AOD9604’s Phase IIb
investigators looked at females in the trial with ‘low response to the diet and
exercise before randomisation’7 the result was ‘similar effect sizes to those
reported in the previous trial’, that trial being a Phase IIb trial which had shown
good performance for low doses of the drug. It’s well known that physical
exercise results in the body producing growth hormone8, and that would
potentially explain why AOD9604, as a growth hormone derivative, failed to
produce much response across most treatment groups where exercise
compliance was better – the drug didn’t ‘synergise’ an exercise programme in
terms of overall body weight, as Metabolic had hoped prior to initiating the trial. It
did, however, burn fat9. We think this data partly confirmed what Metabolic had
observed in February 2002 when it reported results of its first Phase IIa of
AOD9604, where patients registered an increase in fat breakdown 2 hours after
AOD9604 dosing compared to placebo. Patients over 35 showing a 25% increase
in blood levels of non-esterified fatty acids (NEFA) compared to placebo, with a p
value of less than 0.01. This trial, in 23 obese subjects, saw AOD9604
administered intravenously.
In vivo data suggests that AOD9604 can burn fat when it reaches the sites
of fat storage. Two papers from scientists working with Metabolic in Frank Ng’s
lab established in vivo evidence that AOD9604 could stimulate lipolysis:
• The 2000 Hormone Research10 paper. This paper looked at oral treatment of
obese rats with AOD9604, where the drug reduced weight gain over a 19 day
period by over 50% compared to the controls. When the adipose tissues of
the rats were studied the scientists found ‘an increase in lipolytic activity’,
that is, it was fat and not some other tissue that was burned.
• The 2001 Endocrinology11 paper. This paper identified a potential mechanism
of action for AOD9604. The drug, when administered to ob/ob mice
intraperitoneally over a 14 day period, not only saw marked weight losses in
the mice, but also a noticeable increased in the level of expression of Β3
adrenergic receptors whose major function of these receptors is
enhancement of lipolysis.


Also,

AOD9604’s delivery could have been the key issue. POH’s basic thinking on
AOD9604 is that the drug failed because it was made orally available, which likely
reduced bioavailability and also potentially resulted in protein denaturisation in
the gastrointestinal tract, which would have reduced the drug’s activity.
• The molecule was too unwieldy to be a pill - At a molecular weight of 1,815
daltons, AOD9604 is a large drug, around five or six times the size of a typical
small molecule. Drugs much smaller have low oral bioavailability due to
difficulty in getting through the gut wall. For example, leuprolide is a synthetic
nine amino acid peptide with a 1,200 dalton molecular weight used in the
treatment of prostate cancer in men and endometriosis in women. That drug
has virtually no oral bioavailability and has to be delivered through injectable,
injectable depot or subcutaneous implant formats. Even if AOD9604 was
only a small peptide, it would still be susceptible to enzymatic degradation in
the gut, being derived as it is from a naturally occurring protein12.
• Some drug, but probably not enough, got through - For AOD9604, large
molecule size wouldn’t have reduced bioavailability to zero, and the use of
polyethylene glycol as an excipient may have increased bioavailability
slightly13, however there is the distinct possibility that not enough of the drug
got through the gastrointestinal tract to make a therapeutic difference.
• There is evidence that injecting the drug works better – Looking at the charts
which Ng et al. disclosed on AOD9604’s activity in WO 99/12969 (the basic
patent application for the drug), it appears that intraperitoneal injections of
the drug were more effective than oral gavage, with injections showing
weight losses, and oral gavage showing merely slowing of weight gain14.
• POH would further argue that if insulin, three times the size of AOD9604, can
be delivered transdermally via TPM, then successful transdermal delivery of
AOD9604 is not a problem15.
  #6  
Old 04-19-2011, 05:13 AM
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never heard of it, very interesting
  #7  
Old 04-19-2011, 06:21 AM
Goldenchook Goldenchook Is Off Line
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Big B, how would you judge if something new like this was effective or just another snake oil cream.

Seems to have a lot of science behind it.

I have looked at the company web site, and it seems the product is pitched as a cosmetic rather than a medication to reduce fat.

Do things in the body building world based on word of mouth from trial and error, or is there a main "database" you can refer to, to see if things are rubbish or not.
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Old 04-22-2011, 01:48 AM
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Sounds interesting, can you provide a link or more information so we can investigate the product ourselves. TW

PS First times poster. Keep up the good work this is exactly the sort of cutting edge info I came onto this site to get.
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Old 04-22-2011, 06:36 AM
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No problems Tony.
The link to the company selling it is -
Look under body shaper.
They seem to be selling it as a cosmetic but this second link is a news release about the product containing AOD-9604.


Would still like to some feedback on whether people rate AOD-9604.


links edited -if you wish to advertise - contact basskiller
  #10  
Old 04-22-2011, 07:17 AM
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Do you really think I can't see whats going on? Using your friends to push a product or site..


You guys are friends on facebook .. so don't act like you don't know each other
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