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Fertilized Egg

ABSORPTION PROFILE AND HORMONAL INFLUENCES OF Fertilized EGG YOLK INGESTION IN THE HUMAN
Journal of the American College of Nutrition, Volume 25, Number 5, October 2006
Colker, C. Peak Wellness, Inc. Greenwich, CT

Fertile egg yolks contain significant concentrations of follistatin. In an effort to identify whether this orally ingested source of naturally occurring follistatin is actually absorbed and pharmacokinetically active in the human model, this study was undertaken.

A male subject was chosen because the normal baseline male physiology does not regularly contain any measurable concentration of follistatin. Follistatin-rich fertile egg yolk powder properly processed to preserve active follistatin (FolstaxanTM) was obtained (Celldyne Biopharma, San Antonio, TX). After initial blood draw and subsequential oral Folstaxan dosing, serum follistatin levels were qualitatively and quantitatively) measured as an indicator of absorption. In addition, since we know follistatin is a negative modulator of myostatin, serum myostatin levels were qualitatively and quantitatively measured as an indication of hormonal influence and thus true pharmacokinetic activity. Testing utilized purchased follistatin and myostatin standardized for verification. Confirmations were run by ELISA and quantitations by Liquid Chromatography Tandem Mass Spectrometer with third degree fragmentation (Expertox, Deer Park, TX).

Results showed as predicted, a zero level of follistatin at baseline with a myostatin level of 46 pg/ml, 12 hours after FolstaxanTM dosing. Serum follistatin measured 57.1 pg/ml with a decline of myostatin to 34 pg/m1, 24 hours after the initial dosing, follistatin levels began to predictably drop from the time of initial dosing to 11.4 pg/ml. Yet myostatin continued to decline slightly with a 24-hour level of 31 pg/ml. These results clearly indicate that a fertile egg yolk powder properly processed to preserve active follistatin, when orally ingested, results in detectable serum follistatin. Furthermore, this resultant follistatin presence has significant pharmacokinetic activity is shown by the hormonal down regulation of serum follistatin

Follistatin complexes Myostatin and antagonises Myostatin-mediated inhibition of myogenesis.

Amthor H, Nicholas G, McKinnell I, Kemp CF, Sharma M, Kambadur R, Patel K.

Department of Veterinary Basic Sciences, Royal Veterinary College, London NW1 OTU, UK.


Follistatin is known to antagonise the function of several members of the TGF-beta family of secreted signalling factors, including Myostatin, the most powerful inhibitor of muscle growth characterised to date. In this study, we compare the expression of Myostatin and Follistatin during chick development and show that they are expressed in the vicinity or in overlapping domains to suggest possible interaction during muscle development. We performed yeast and mammalian two-hybrid studies and show that Myostatin and Follistatin interact directly. We further show that single modules of the Follistatin protein cannot associate with Myostatin suggesting that the entire protein is required for the interaction. We analysed the interaction kinetics of the two proteins and found that Follistatin binds Myostatin with a high affinity of 5.84 x 10(-10) M. We next tested whether Follistatin suppresses Myostatin activity during muscle development. We confirmed our previous observation that treatment of chick limb buds with Myostatin results in a severe decrease in the expression of two key myogenic regulatory genes Pax-3 and MyoD. However, in the presence of Follistatin, the Myostatin-mediated inhibition of Pax-3 and MyoD expression is blocked. We additionally show that Myostatin inhibits terminal differentiation of muscle cells in high-density cell cultures of limb mesenchyme (micromass) and that Follistatin rescues muscle differentiation in a concentration-dependent manner. In summary, our data suggest that Follistatin antagonises Myostatin by direct protein interaction, which prevents Myostatin from executing its inhibitory effect on muscle development.

ABSORPTION PROFILE AND HORMONAL INFLUENCES OF Fertilized EGG YOLK INGESTION
IN THE HUMAN
Colker. C. Peak Wellness, Inc. Greenwich, CT


Fertile egg yolks contain significant concentrations of follistatin. In an
effort to identify whether this orally ingested source of naturally
occurring follistatin is actually absorbed and pharmacokinetically active in
the human model, this study was undertaken. A male subject was chosen
because the nornma1basline male physiology does not regularly contain any
measurable concentration of follistatin. Follistatin-rich fertile egg yolk
powder properly processed to preserve active follistatin (FolstaxanTM) was
obtained (Celldyne Biopharma, San Antonio, TX). After initial blood draw and
subsequential oral Folstaxan dosing, serum follistatin levels were
qualitatively and quantitatively) measured as an indicator of absorption. In
addition, since we know follistatin is a negative modulator of myostatin,
serum myostatin levels were qualitatively and quantitatively measured as an
indication of hormonal influence and thus true pharmacokinetic activity.
Testing utilized purchased follistatin and myostatin standardized for
verification. Confirmations were run by ELISA and quantitations by Liquid
Chromatography Tandem Mass Spectrometer with third degree fragmentation
(Expertox, Deer Park, TX). Results showed as predicted, a zero level of
follistatin at baseline with a myostatin level of 46 pg/ml, 12 hours after
FolstaxanTM dosing. Serum follistatin measured 57.1 pg/ml with a decline of
myostatin to 34 pg/m1, 24 hours after the initial dosing, follistatin levels
began to predictably drop from the time of initial dosing to 11.4 pg/ml. Yet
myostatin continued to decline slightly with a 24-hour level of 31 pg/ml.
These results clearly indicate that a fertile egg yolk powder properly
processed to preserve active follistatin, when orally ingested, results in
detectable serum follistatin. Furthermore, this resultant follistatin
presence has significant pharmacokinetic activity is shown by the hormonal
down regulation of serum follistatin.