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Effects of Recombinant Human Insulin-Like Growth Factor I Administration on Spontaneous and Growth Hormone (GH)-Releasing Hormone-Stimulated GH Secretion in Anorexia Nervosa¹

Division of Endocrinology (L.G., E.A., F.L., E.G.), Department of Internal Medicine, University of Turin, 10126 Turin; Second Chair of Endocrinology (A.I.P., M.S., F.C.), University of Milan, San Luca Hospital, 20149 Milano; Unit of Adolescentology (M.R., D.B.), University of Pisa, 56100 Pisa; and Department of Pharmacology (A.T., E.E.M.), University of Milan, 20129 Milano, Italy

Address correspondence and requests for reprints to: Prof. E. E. Muller, Department of Pharmacology, University of Milan, Via Vanvitelli 32, Milano, Italy. E-mail: eugenio.muller{at}unimi.it

Exaggerated GH and reduced insulin-like growth factor I (IGF-I) levels are common features in anorexia nervosa (AN). A reduction of the negative IGF-I feedback could account, in part, for GH hypersecretion. To ascertain this, we studied the effects of recombinant human (rh)IGF-I on spontaneous and GH-releasing hormone (GHRH)-stimulated GH secretion in nine women with AN [body mass index, 14.1 ± 0.6 kg/m²] and in weight matched controls (normal weight). Mean basal GH concentrations (mGHc) and GHRH (2.0 µg/kg, iv) stimulation were significantly higher in AN. rhIGF-I administration (20 µg/kg, sc) significantly reduced mGHc in AN (P < 0.01), but not normal weight, and inhibited peak GH response to GHRH in both groups; mGHc and peak GH, however, persisted at a significantly higher level in AN. Insulin, glucose, and IGFBP-1 basal levels were similar in both groups. rhIGF-I inhibited insulin in AN, whereas glucose remained unaffected in both groups. IGFBP-1 increased in both groups (P < 0.05), with significantly higher levels in AN. IGFBP-3 was under basal conditions at a lower level in AN (P < 0.05) and remained unaffected by rhIGF-I. This study demonstrates that a low rhIGF-I dose inhibits, but does not normalize, spontaneous and GHRH-stimulated GH secretion in AN, pointing also to the existence of a defective hypothalamic control of GH release. Moreover, the increased IGFBP-1 levels might curtail the negative IGF-I feedback in AN.

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