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Consistent with this, patients with T2D responded to IGF-1 treatment with improved glucose tolerance, hyperinsulinaemia, and hyperlipidaemia as previously stated [280]

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Of course

Samples were tested for the presence of AIs (2-androstenol (5-androst-2-en-17-ol), 2-androstenone (5-androst-2-en-17-one), 3-androstenol (5-androst-3-en-17-ol), 3-androstenone (5-androst-3-en-17-one), 4-androstene-3,6,17 trione (6-oxo), aminoglutethimide, anastrozole, androsta-1,4,6-triene-3,17-dione (androstatrienedione), androsta-3,5-diene-7,17-dione (arimistane), exemestane, formestane, letrozole, and testolactone), and anti-estrogenic substance (bazedoxifene, clomiphene, cyclofenil, fulvestrant, ospemifene, raloxifene, tamoxifen, and toremifene) prohibited by WADA

Complementary to the above, it has been thought for a long time that only supraphysiological concentrations of IGF-1 are able to activate the IR, as will be further discussed in this manuscript