Long R3 insulin-like growth factor-I (IGF-I) infusion stimulates organ growth but reduces plasma IGF-I, IGF-II and IGF binding protein concentrations in the guinea pig. — VialBase Research
The only IGF-1-LR3 evidence here is animal data, and it directly contradicts the marketing premise that LR3 raises systemic IGF: organ growth increased while plasma IGF-I, IGF-II and IGF binding protein concentrations fell and whole-body growth did not change.
- Female guinea pigs (350 g body weight) were continuously infused for 7 days with recombinant guinea pig IGF-I or IGF-II (120 or 360 micrograms/day) or Long R3 IGF-I (120 micrograms/day), an analogue with much reduced affinities for IGF binding proteins
- Long R3 IGF-I significantly increased the fractional weight (g/kg body weight) of adrenals, gut, kidneys and spleen, but overall body growth was not stimulated
- Body weight gain, feed intake, feed conversion efficiency and carcass composition were not significantly affected by any treatment (significance threshold P < 0.05)
- Per the study's stated conclusion in its title, Long R3 IGF-I infusion reduced plasma IGF-I, IGF-II and IGF binding protein concentrations
- Total circulating IGF concentrations were not increased by these treatments; the authors offer this as the likely explanation for the absence of whole-body growth effects
Summary
This is an animal study in guinea pigs — there is no human data in it. The authors set out to test whether an animal carrying substantial amounts of both IGF-I and IGF-II in circulation (the guinea pig) responds to chronic IGF infusion the same way the adult rat does, since the rat has negligible circulating IGF-II. Female guinea pigs of 350 g body weight were continuously infused for 7 days with recombinant guinea pig IGF-I or IGF-II (120 or 360 micrograms/day) or with Long R3 IGF-I (LR3IGF-I) at 120 micrograms/day, described in the paper as an analogue with much reduced affinities for IGF binding proteins. Infusing native IGF-I or IGF-II substantially raised plasma IGF-I or IGF-II respectively versus vehicle, yet body weight gain, feed intake, feed conversion efficiency and carcass composition were not significantly affected by any treatment. Among the tissues examined, only adrenal fractional weight rose with the higher (360 micrograms/day) IGF-I dose, whereas LR3IGF-I significantly increased the fractional weight of adrenals, gut, kidneys and spleen — again without stimulating overall growth. The authors propose that the lack of whole-body IGF-I effect is explained by total circulating IGF concentrations not being increased by these treatments; IGF-II raised total IGF only at the higher dose, plasma IGF-I fell with IGF-II infusion, and plasma IGF-II fell with IGF-I infusion. The paper’s title states the corresponding finding for the analogue: Long R3 IGF-I infusion stimulated organ growth but reduced plasma IGF-I, IGF-II and IGF binding protein concentrations. The available abstract is truncated at 250 words, so the numerical detail behind that title claim is not reproduced here.
Key Findings
- Design: 7-day continuous infusion in female guinea pigs (350 g) of recombinant guinea pig IGF-I or IGF-II at 120 or 360 micrograms/day, or Long R3 IGF-I at 120 micrograms/day, versus vehicle-infused controls
- Long R3 IGF-I significantly increased the fractional weight (g/kg body weight) of adrenals, gut, kidneys and spleen — organ-selective growth, not systemic growth
- No treatment significantly affected body weight gain, feed intake, feed conversion efficiency or carcass composition (P < 0.05 significance threshold) — the outcomes closest to what LR3 is marketed for showed nothing
- The paper’s title reports that Long R3 IGF-I infusion reduced plasma IGF-I, IGF-II and IGF binding protein concentrations, i.e. administering the analogue lowered rather than raised measured circulating IGF
- Native IGF-I and IGF-II infusions raised their own plasma concentrations but suppressed the other IGF (plasma IGF-I fell with IGF-II infusion and vice versa), and total circulating IGF was not increased — the authors’ proposed explanation for the absent growth response
- LR3 IGF-I is characterised in this paper as having much reduced affinity for IGF binding proteins, the pharmacological property that distinguishes it from native IGF-I
Relevance to IGF-1-LR3
This is animal evidence only — guinea pigs, 7 days, no human subjects — and that limitation should travel with every claim drawn from it. Within that limit it is one of the more useful counterweights to the way IGF-1-LR3 is marketed: the assumption behind “more IGF is better” is that administering a binding-protein-resistant analogue drives circulating IGF up and lean tissue with it. Here the opposite pattern was reported. Long R3 IGF-I produced selective growth of adrenals, gut, kidneys and spleen — visceral organs, not skeletal muscle — while the study title reports plasma IGF-I, IGF-II and IGF binding protein concentrations were reduced, and body weight gain and carcass composition did not budge. Anyone reading vendor claims about LR3 driving systemic anabolism should weigh the fact that in this model the compound grew organs, not the animal, and appears to have suppressed the very biomarkers users are told it elevates.
Citation
Conlon MA, Tomas FM, Owens PC, et al. Long R3 insulin-like growth factor-I (IGF-I) infusion stimulates organ growth but reduces plasma IGF-I, IGF-II and IGF binding protein concentrations in the guinea pig. The Journal of endocrinology. 1995;146(2):247-53. doi:10.1677/joe.0.1460247.
See Also
- Parent compound: IGF-1-LR3
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