Prostaglandin F2alpha is a potent inhibitor of adipocyte precursor differentiation and a physiological negative modulator of adipocyte function (ie triglyceride accumulation) through stimulation of transforming growth factor-alpha mRNA expression. It initiates a cascade of effects in the adipoctes which have physiological importance to reducing the size and it appears number of mature cells,long after PGf-2a is cleared from the system
Mature adipose cells only shrink in size in response to restricted caloric intake or increased metabolic demand. Before now the only method of reducing the number of fat cells was liposuction. It now appears that Pgf-2a applied topically can have the same same effecst as diet and liposuction. Pgf-2a can reduce the size of mature adipocytes and the number of mature adipocytes through negative modulation and reversing the process of differentiation
There are no studies on topical application. DMSO does carry PGF-2a through the dermal layers and the low concentration spread over a large area is ideal for the intended purpose. One cannot spread PGf-2a (or anyother substance) over the surface area that one can with DMSO topical application. The idea being that you need to interact as many molecules of PGF-2a with as many mature fat cells as possible. The biggest asset to DMSO as a carrier is the ability to spread the PGF-2a applicatiion over a large surface area, thereby maximising the interactuion of the number PGF-2a molucules with the maximum number of fat cells. This is where the DMOS method really shines. QFS is not masking the smell of the DMSO. It is not that bad and goes away in about 5 minutes.
It is important to remember that dinoprost tromethamine does not burn the released fatty acids, aerobic exercise and or T3 will take care of that. PGF-2a only changes the way fats are stored and the formation and function of adipose tissue. As well I find that about half of the time I feel a tickle in the back of my throat and sometimes I have a full out coughing fit. This says to me that I have applied a good dosage.
Here are some studies that support PGF-2a and negative modulation of adipose tissue.
Endocrinology 1995 Aug;136(8):3222-9
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.
Int J Obes Relat Metab Disord 1996 Mar;20 Suppl 3:S58-64 R
Endocrine and paracrine negative regulators of adipose differentiation.
Serrero G, Lepak N.
W Alton Jones Cell Science Center, Inc, Lake Placid, NY 12946, USA.
Obesity which is characterized by an abnormal adipose tissue development is a first degree public health hazard in industrialized countries. One important aspect in the study of adipose tissue development is to investigate the hormonal control of proliferation and differentiation. Any qualitative or quantitative change in these hormones or their receptors can result in abnormalities in the process of proliferation and/or differentiation possibly leading to obesity. Therefore, it is important to identify these factors and investigate their mechanism of action. We have concentrated our efforts in the study of factors triggering differentiation (positive regulators) and also of factors inhibiting differentiation (negative regulators). The present paper provides evidence of the importance of EGF/TGF-alpha and of PGF2 alpha as differentiation inhibitors for adipocyte precursors in primary culture. Data presented here also demonstrate that TGF-alpha is expressed in adipose tissue and that its expression is specifically stimulated by PGF2 alpha, thus suggesting the existence of an amplification mechanism between two differentiation inhibitors within the adipose tissue. The importance of these two types of differentiation inhibitors in the regulation of adipose tissue development is discussed.