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Growth Hormone (GH) Response to GH-Releasing Peptide-6 in Type 1 Diabetic Patients with Exaggerated GH-Releasing Hormone-Stimulated GH Secretion¹

Departments of Endocrinology, Montecelo Hospital, Pontevedra (P.F.C.), and Xeral-Cíes Hospital, Vigo (M.A.A., R.V.G.-M.). Department of Functional Biology and Health Sciences, University of Vigo (F.M.); and Department of Physiology, University of Santiago de Compostela (C.D.); Spain.

Address all correspondence and requests for reprints to: Federico Mallo, Department of Functional Biology and Health Sciences, Faculty of Sciences, Campus of Vigo, University of Vigo, Vigo, Spain E-36.200.

In type 1 diabetes mellitus (DM 1), high GH basal levels and exaggerated GH responses to several stimuli, including GHRH, have been described. GH-releasing peptide-6 (GHRP-6) is a synthetic hexapeptide that specifically stimulates GH release, both in vitro and in vivo.

The aim of this study was to evaluate the effects of GHRP-6 alone or in combination with GHRH on GH secretion in DM 1. Six type 1 diabetic males and six age-, sex-, and body mass index-matched control volunteers were studied. Each subject received GHRH (100 µg iv), GHRP-6 (90 µg iv), and GHRH plus GHRP-6 on three separate days. GH peak values were higher in DM 1 patients than in control volunteers, after GHRH (52.2 ± 9.8 vs. 19.3 ± 6.0 µg/L; P = 0.016), GHRP-6 (66.2 ± 9.6 vs. 39.9 ± 6.3 µg/L; P = 0.05), and GHRH plus GHRP-6 (81.8 ± 4.4 vs. 53.7 ± 8.2 µg/L; P = 0.01). An additive GH response to combined administration of these two peptides was observed in diabetic patients. Serum insulin-like growth factor (IGF)-1 levels were diminished in DM 1, with respect to normal subjects (145.2 ± 21.5 vs. 269.7 ± 42.0 µg/L; P = 0.01), whereas IGF-binding protein-3 levels were not significantly different between DM-1 and controls.

In summary, GHRP-6 is a potent stimulus for GH secretion in DM 1. The combined administration of GHRP-6 plus GHRH constitutes the most powerful stimulus for GH secretion in DM 1. These patients exhibit a greater GH secretory capacity than normal subjects, probably caused by a diminished tone in the IGF-1 sustained negative feedback control exerted upon somatotroph responsiveness.

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