irishpride
MuscleChemistry Registered Member
Ok bros i wanna hear some first hand info on PGF2..results,sides doses everything you guys can give me on this please do..thanks
First Hand PGF2 info wanted
- Thread starter irishpride
- Start date
I have done PGF2a with IGF-1 and I have done PGF2a with AAS. I would think that it does increase growth slightly. I found that .3ml at one time is a pretty good dose as far as sides go and a max of .5ml at one time, at those dosages inject atleast 3 times a day 5 or 6 would be better. You will feel like you need to take a shit even at those dosages. Ive done a 2ml dose before.....stupid stupid stupid....I felt very hot, sweating, sick, shitting like crazy, all I could think about was getting it over with.
irishpride
MuscleChemistry Registered Member
so Cordoba do you think its worth it??? was there any fat lose??also did you feel dehydrated with the shittin your brains out LOL...thanks for the help and how long did you stay on??Cordoba said:
If you can get it cheap give it a shot, but I wouldnt spend allot of money on it. I have two more bottles and I think I will use them on my long break from AAS to try to preserve some muscle mass. I didnt notice any fat loss. I was never dehydrated but I drink allot of water.
EatingMachine
New member
How about transdermal use for fat loss? Does it work?
I don't have much desire to sit on the can all day from using IM.
I don't have much desire to sit on the can all day from using IM.
proud13
New member
Painful hell yeah!! Sides suck big time!!
Effective hell yeah will shred you up incredibly. Look into something called arochidonic acid though. It's a patent pending product (OTC=legal) and it causes the same thing as PGF to a lesser extent.
I've used it and noticed the constriction of airway, uncomfortable stomach and increased body temp while taking 4 pills at once on an empty stomach. I'll post a link to some info on it below.
Effective hell yeah will shred you up incredibly. Look into something called arochidonic acid though. It's a patent pending product (OTC=legal) and it causes the same thing as PGF to a lesser extent.
I've used it and noticed the constriction of airway, uncomfortable stomach and increased body temp while taking 4 pills at once on an empty stomach. I'll post a link to some info on it below.
proud13
New member
http://www.molecularnutrition.net/X_factor.htm
Unfortunately only one company makes the product but this site gives a description of what it does. However, I def. don't believe their advertising which states it is the strongest, legal non-steroidal compound available.
Does it work? I would assume by the reading, the references of studies which most of I read and the fact I used it and noticed similar efx to that of a low dose of PGF-2alpha. Nonetheless the above site is cool reading.
Unfortunately only one company makes the product but this site gives a description of what it does. However, I def. don't believe their advertising which states it is the strongest, legal non-steroidal compound available.
Does it work? I would assume by the reading, the references of studies which most of I read and the fact I used it and noticed similar efx to that of a low dose of PGF-2alpha. Nonetheless the above site is cool reading.
proud13
New member
Eating machine,
I've never tried transdermally however, I would think it could possibly be more effective if it were to only affect topically. Yet the way it helps you lose fat is by the incredible increase in body temp which is often accustomed by goose bumps since the body doesn't recognize the immediate change and behaves oddly.
QFS had a trans. product but are no longer in biz. It sounded interesting though in the way they prepared it.
I've never tried transdermally however, I would think it could possibly be more effective if it were to only affect topically. Yet the way it helps you lose fat is by the incredible increase in body temp which is often accustomed by goose bumps since the body doesn't recognize the immediate change and behaves oddly.
QFS had a trans. product but are no longer in biz. It sounded interesting though in the way they prepared it.
irishpride
MuscleChemistry Registered Member
thanks cy
proud13
New member
Here is a study done on that fatty acid I was referring to.
Autocrine control of adipose cell differentiation by prostacyclin and PGF2 alpha.
Catalioto RM, Gaillard D, Maclouf J, Ailhaud G, Negrel R.
Centre de Biochimie (CNRS UPR 7300), Faculte des Sciences, Universite de Nice-Sophia Antipolis, France.
The mitogenic-adipogenic effect exerted by arachidonic acid, which leads to terminal differentiation of Ob1771 mouse preadipocytes, has been shown to be (i) blocked by cyclooxygenase inhibitors, (ii) mimicked by a stable analogue of prostacyclin (carbaprostacyclin) and (iii) potentiated by PGF2 alpha. Since these prostanoids are known to be synthesized and secreted by preadipocytes, we have proposed that both prostacyclin as the key mediator and PGF2 alpha as a modulator control the expression of terminal events of adipose conversion by means of an autocrine mechanism (Gaillard, D. et al. and Negrel, R. et al. Biochem. J. (1989) 257, 389-397 and 399-405). In order to test this hypothesis, the release of prostacyclin, characterized under the form of its stable degradation product 6-keto-PGF1 alpha, and that of PGF2 alpha have been studied in the culture medium of Ob1771 cells. A striking increase in the release of 6-keto-PGF1 alpha and to a minor degree of PGF2 alpha was observed when cells were exposed to arachidonic acid as shown by using [3H]arachidonic acid prelabelled cells or by radio-immunoassays. Since antagonists of PGF2 alpha and PGI2 receptors were not available, specific antibodies directed against PGF2 alpha and 6 beta-PGI1, another stable analogue of prostacyclin, were added as neutralizing agents in the culture medium. These antibodies were able to counteract the mitogenic-adipogenic effect of arachidonic acid. Prostacyclin and PGF2 alpha thus appear as autocrine mediators in the process of adipose conversion.
Autocrine control of adipose cell differentiation by prostacyclin and PGF2 alpha.
Catalioto RM, Gaillard D, Maclouf J, Ailhaud G, Negrel R.
Centre de Biochimie (CNRS UPR 7300), Faculte des Sciences, Universite de Nice-Sophia Antipolis, France.
The mitogenic-adipogenic effect exerted by arachidonic acid, which leads to terminal differentiation of Ob1771 mouse preadipocytes, has been shown to be (i) blocked by cyclooxygenase inhibitors, (ii) mimicked by a stable analogue of prostacyclin (carbaprostacyclin) and (iii) potentiated by PGF2 alpha. Since these prostanoids are known to be synthesized and secreted by preadipocytes, we have proposed that both prostacyclin as the key mediator and PGF2 alpha as a modulator control the expression of terminal events of adipose conversion by means of an autocrine mechanism (Gaillard, D. et al. and Negrel, R. et al. Biochem. J. (1989) 257, 389-397 and 399-405). In order to test this hypothesis, the release of prostacyclin, characterized under the form of its stable degradation product 6-keto-PGF1 alpha, and that of PGF2 alpha have been studied in the culture medium of Ob1771 cells. A striking increase in the release of 6-keto-PGF1 alpha and to a minor degree of PGF2 alpha was observed when cells were exposed to arachidonic acid as shown by using [3H]arachidonic acid prelabelled cells or by radio-immunoassays. Since antagonists of PGF2 alpha and PGI2 receptors were not available, specific antibodies directed against PGF2 alpha and 6 beta-PGI1, another stable analogue of prostacyclin, were added as neutralizing agents in the culture medium. These antibodies were able to counteract the mitogenic-adipogenic effect of arachidonic acid. Prostacyclin and PGF2 alpha thus appear as autocrine mediators in the process of adipose conversion.
proud13
New member
Another...basically stating that PGF2-alpha eats fat and prevents others from forming...
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Prostaglandin F2 alpha stimulates transforming growth factor-alpha expression in adipocyte precursors.
Lepak NM, Serrero G.
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946, USA.
Transforming growth factor-alpha (TGF alpha) and prostaglandin F2 alpha (PGF2 alpha) are potent inhibitors of adipocyte differentiation. We demonstrate here that TGF alpha messenger RNA (mRNA) is expressed in freshly isolated fat pads and in primary culture of adipocyte precursors cultivated in defined medium before and after differentiation. We show that PGF2 alpha stimulated TGF alpha mRNA expression in a dose-dependent manner. PGF2 alpha also stimulated TGF alpha production in the culture medium of adipocyte precursors in primary culture. PGF2 alpha stimulated TGF alpha mRNA expression in both undifferentiated and differentiated cells. 9 alpha,11 beta-PGF2 alpha, which also inhibited adipose differentiation, stimulated TGF alpha mRNA expression similarly to PGF2 alpha, whereas other PGs had no effect on TGF alpha mRNA expression. The time-course experiment indicates that the stimulation of TGF alpha mRNA expression by PGF2 alpha is observed within 6 h of exposure to PGF2 alpha and is inhibited by treatment of the cells with actinomycin D. The effect of PGF2 alpha on TGF alpha expression did not require activation of protein kinase C and was fully reversible. As both TGF alpha and PGF2 alpha are inhibitors of adipose differentiation, it is suggested that stimulation of TGF alpha expression by PGF2 alpha could represent an amplification mechanism to modulate adipocyte precursor differentiation and adipocyte function within the adipose tissue.
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Prostaglandin F2 alpha stimulates transforming growth factor-alpha expression in adipocyte precursors.
Lepak NM, Serrero G.
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946, USA.
Transforming growth factor-alpha (TGF alpha) and prostaglandin F2 alpha (PGF2 alpha) are potent inhibitors of adipocyte differentiation. We demonstrate here that TGF alpha messenger RNA (mRNA) is expressed in freshly isolated fat pads and in primary culture of adipocyte precursors cultivated in defined medium before and after differentiation. We show that PGF2 alpha stimulated TGF alpha mRNA expression in a dose-dependent manner. PGF2 alpha also stimulated TGF alpha production in the culture medium of adipocyte precursors in primary culture. PGF2 alpha stimulated TGF alpha mRNA expression in both undifferentiated and differentiated cells. 9 alpha,11 beta-PGF2 alpha, which also inhibited adipose differentiation, stimulated TGF alpha mRNA expression similarly to PGF2 alpha, whereas other PGs had no effect on TGF alpha mRNA expression. The time-course experiment indicates that the stimulation of TGF alpha mRNA expression by PGF2 alpha is observed within 6 h of exposure to PGF2 alpha and is inhibited by treatment of the cells with actinomycin D. The effect of PGF2 alpha on TGF alpha expression did not require activation of protein kinase C and was fully reversible. As both TGF alpha and PGF2 alpha are inhibitors of adipose differentiation, it is suggested that stimulation of TGF alpha expression by PGF2 alpha could represent an amplification mechanism to modulate adipocyte precursor differentiation and adipocyte function within the adipose tissue.
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