title: Effects of recombinant human insulin-like growth factor I administration on spontaneous and growth hormone (GH)-releasing hormone-stimulated GH secretion in anorexia nervosa.
abstract: 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 microg/kg, iv) stimulation were significantly higher in AN. rhIGF-I administration (20 microg/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.
authors.affiliation: Department of Internal Medicine, University of Turin, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Gianotti
authors.forename: A I
authors.initials: AI
authors.lastname: Pincelli
authors.forename: M
authors.initials: M
authors.lastname: Scacchi
authors.forename: M
authors.initials: M
authors.lastname: Rolla
authors.forename: D
authors.initials: D
authors.lastname: Bellitti
authors.forename: E
authors.initials: E
authors.lastname: Arvat
authors.forename: F
authors.initials: F
authors.lastname: Lanfranco
authors.forename: A
authors.initials: A
authors.lastname: Torsello
authors.forename: E
authors.initials: E
authors.lastname: Ghigo
authors.forename: F
authors.initials: F
authors.lastname: Cavagnini
authors.forename: E E
authors.initials: EE
authors.lastname: Müller
mesh_terms: D000293:Adolescent; D000328:Adult; D000856:Anorexia Nervosa / Q000097:blood / Q000503:physiopathology*; D001786:Blood Glucose / Q000378:metabolism; D004958:Estradiol / Q000097:blood; D005246:Feedback; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D013007:Growth Hormone-Releasing Hormone / Q000008:administration & dosage / Q000494:pharmacology*; D019382:Human Growth Hormone / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007279:Injections, Subcutaneous; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000097:blood; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000494:pharmacology; D012016:Reference Values
chemical_list: D001786:Blood Glucose; D007328:Insulin; D018970:Insulin-Like Growth Factor Binding Protein 1; D011994:Recombinant Proteins; D019382:Human Growth Hormone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013007:Growth Hormone-Releasing Hormone