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I challenge you - test our IGF1 (somedin)

sciroxx-lab

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Not for my best knowledge, from what I know it's used to help prolifiration of certain bacteria in the biotech industry.

Of course it's very usable for anabolic purposes for humans, and numerous reports here and on many forum (search Somedin) have proven this
 
Not for my best knowledge, from what I know it's used to help prolifiration of certain bacteria in the biotech industry.

Of course it's very usable for anabolic purposes for humans, and numerous reports here and on many forum (search Somedin) have proven this
I recall reading somewhere that it was theorised that lactic acid build up in the working muscle tissue might alter endogenous IGF-1 such that it turned it into DES 1-3 IGF-1... Will have to look it up again.

If it was ever proven true, then this molecule is actually produced in humans under specific circumstances (acidosis). The autocrine / paracrine systems (or pathways) are even more complex than the endocrine system and the interplay (for lack of a better word) between small molecules and larger growth factors / enzymes / proteins is not fully understood.

As an aside, I notice lots of people typing IGF LR3 when it is actually LR3 IGF-1 -- a synthetic form never found / produced in humans. As far as i have read, LR3 was specifically developed for certain conditions.

The same goes for 'DES'; it is DES 1-3 IGF-1, not IGF-1 DES. I guess I'm being picky about nomenclature [emoji30]

Sent from my Nexus 5 using Tapatalk
 
Here is an abstract from Int J Biochem Cell Biol. 1996 Oct;28(10):1085-7

Abstract

Des(1-3)IGF-I, a truncated variant of human IGF-I with the tripeptide Gly-Pro-Glu absent from the N-terminus, has been isolated from bovine colostrum, human brain and porcine uterus. This protein probably results from post-translational cleavage of IGF-I. Des(1-3)IGF-I generally is about 10-fold more potent than IGF-I at stimulating hypertrophy and proliferation of cultured cells, a consequence of much reduced binding to IGF-binding proteins, in turn caused by the absence of the glutamate at position 3. The increased potency is retained in part when the variant is administered in vivo, with selective anabolic effects particularly evident in gut tissues. Clinical opportunities for des(1-3)IGF-I have not yet been evaluated, but could apply in catabolic states as well as for the treatment of inflammatory bowel diseases.

PMID: 8930132 (pubmed ID)

This demonstrates that the compound is found in humans (human brain tissue in this study) but does not mention how it is produced in vivo -- at least not in the abstract. Will keep looking.

The abstract does mention that it might have therapeutic application for IBS !! [emoji47]



Sent from my Nexus 5 using Tapatalk
 
Very interesting info, and shed some light from the scientific point of view to the anecdote about the dramatic prolifiration effect of the DES-IGF1
 
Here is an abstract from Int J Biochem Cell Biol. 1996 Oct;28(10):1085-7

Abstract

Des(1-3)IGF-I, a truncated variant of human IGF-I with the tripeptide Gly-Pro-Glu absent from the N-terminus, has been isolated from bovine colostrum, human brain and porcine uterus. This protein probably results from post-translational cleavage of IGF-I. Des(1-3)IGF-I generally is about 10-fold more potent than IGF-I at stimulating hypertrophy and proliferation of cultured cells, a consequence of much reduced binding to IGF-binding proteins, in turn caused by the absence of the glutamate at position 3. The increased potency is retained in part when the variant is administered in vivo, with selective anabolic effects particularly evident in gut tissues. Clinical opportunities for des(1-3)IGF-I have not yet been evaluated, but could apply in catabolic states as well as for the treatment of inflammatory bowel diseases.

PMID: 8930132 (pubmed ID)

This demonstrates that the compound is found in humans (human brain tissue in this study) but does not mention how it is produced in vivo -- at least not in the abstract. Will keep looking.

The abstract does mention that it might have therapeutic application for IBS !! [emoji47]



Sent from my Nexus 5 using Tapatalk

This is a highly valuable info, first time that I see in a scientific literature that the DES has 10 times higher affinity then the endogenous IGF1.

IGF1 has some very unique anti catabolic traits, that for instance GH by itself doesn't have, so the potential of the DEs-IGF1 is very dramatic for such purposes

Here are some examples for this -

http://www.ncbi.nlm.nih.gov/pubmed/9129466
------------conclusions -
GH and IGF-I combined further enhanced fat oxidation while reducing protein catabolism. Serum insulin concentrations were significantly increased by GH but decreased by IGF-I. GH significantly decreased serum total triiodothyronine concentrations and IGF-I significantly decreased serum corticosterone concentrations.

http://www.ncbi.nlm.nih.gov/pubmed/10571453
-----------results and conclusions
RESULTS:
Administration of IGF-I, but not GH, attenuates dexamethasone-induced protein catabolism and increases insulin sensitivity. Simultaneous treatment with GH and IGF-I additively increases the serum concentration of IGF-I, whole-body anabolism, and lipid oxidation. GH or IGF-I when given alone produces similar increases in the serum concentration of IGF-I. However, GH selectively increases skeletal muscle mass whereas IGF-I selectively attenuates the intestinal atrophy and abnormal intestinal ion transport induced by TPN. These tissue-selective anabolic effects of GH and IGF-I are associated with differential increases in protein synthesis in skeletal muscle and jejunum, respectively.
CONCLUSIONS:
Simultaneous treatment with GH and IGF-I may offer the greatest clinical efficacy because of improved nitrogen retention in association with enhanced lipid oxidation and stimulation of protein synthesis in multiple tissue types.
 
This is a highly valuable info, first time that I see in a scientific literature that the DES has 10 times higher affinity then the endogenous IGF1.

IGF1 has some very unique anti catabolic traits, that for instance GH by itself doesn't have, so the potential of the DEs-IGF1 is very dramatic for such purposes

Here are some examples for this -

http://www.ncbi.nlm.nih.gov/pubmed/9129466
------------conclusions -
GH and IGF-I combined further enhanced fat oxidation while reducing protein catabolism. Serum insulin concentrations were significantly increased by GH but decreased by IGF-I. GH significantly decreased serum total triiodothyronine concentrations and IGF-I significantly decreased serum corticosterone concentrations.

http://www.ncbi.nlm.nih.gov/pubmed/10571453
-----------results and conclusions
RESULTS:
Administration of IGF-I, but not GH, attenuates dexamethasone-induced protein catabolism and increases insulin sensitivity. Simultaneous treatment with GH and IGF-I additively increases the serum concentration of IGF-I, whole-body anabolism, and lipid oxidation. GH or IGF-I when given alone produces similar increases in the serum concentration of IGF-I. However, GH selectively increases skeletal muscle mass whereas IGF-I selectively attenuates the intestinal atrophy and abnormal intestinal ion transport induced by TPN. These tissue-selective anabolic effects of GH and IGF-I are associated with differential increases in protein synthesis in skeletal muscle and jejunum, respectively.
CONCLUSIONS:
Simultaneous treatment with GH and IGF-I may offer the greatest clinical efficacy because of improved nitrogen retention in association with enhanced lipid oxidation and stimulation of protein synthesis in multiple tissue types.

THIS INFO IS EXTREMELY USEFUL!!!
 

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