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Administration of Human Insulin-Like Growth Factor-Binding Protein-1 Increases Circulating Levels of Growth Hormone in Mice

Vesna Cingel-Risti, Johan W. van Neck, Jan Frystyk, Stenvert L. S. Drop and Allan Flyvbjerg

Laboratory of Pediatrics, Subdivision of Molecular Endocrinology (V.C.-R., S.L.S.D.), and Department of Plastic and Reconstructive Surgery (J.W.V.N.), Erasmus Medical Center, 3000 DR Rotterdam, Rotterdam, The Netherlands; and Medical Research Laboratories, Clinical Institute, Aarhus University Hospital (V.C.-R., J.F., A.F.), DK-8000 Aarhus, Denmark

Address all correspondence and requests for reprints to: Dr. Allan Flyvbjerg, Medical Research Laboratories, Clinical Institute, Aarhus University Hospital, DK-8000 Aarhus C., Denmark. E-mail: allan.flyvbjerg{at}dadlnet.dk.

GH is the major regulator of circulating IGF-I, which, in return, controls pituitary GH secretion by negative feedback. IGF-binding protein-1 (IGFBP-1) is believed to modify this feedback through its effects on free IGF-I. In the present study we investigated the potential influence of IGFBP-1 on GH secretion in the absence or presence of a GH receptor antagonist (GHRA) that specifically blocks peripheral GH action. We administered human (h) IGFBP-1 and GHRA to mice alone or in combination for 2 or 7 d. GHRA was administered in a dose previously shown to block GH action without an effect on circulating GH or IGF-I levels. hIGFBP-1 administration increased stimulated circulating GH levels and serum total IGF-I and IGFBP-3 levels. Coadministration of GHRA abolished the hIGFBP-1-induced increase in serum IGF-I and IGFBP-3 levels, whereas stimulated GH levels remained increased. Free IGF-I levels in serum were unchanged in all treatment groups. In conclusion, GH serum levels increased in response to hIGFBP-1 administration, even in the setting of normal IGF-I levels. This finding suggests a direct involvement of IGFBP-1 in GH secretion.

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