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Pattern-Dependent Suppression of Growth Hormone (GH) Pulsatility by Ghrelin and GH-Releasing Peptide-6 in Moderately GH-Deficient Rats

Cardiff School of Biosciences (N.M.T., J.S.D., T.W.), Cardiff University, Cardiff CF10 3US, United Kingdom; Department of Medical Nutrition (A.M.), Karolinska Institutet, Huddinge University Hospital, Novum S-14186, Sweden; and Department of Neuroendocrinology (P.A.H.), Division of Neuroscience and Psychological Medicine, Imperial College London, Hammersmith Hospital, London W12 0NN, United Kingdom

Address all correspondence and requests for reprints to: Dr. Timothy Wells, School of Biosciences, Cardiff University, P.O. Box 911, Museum Avenue, Cardiff CF10 3US, United Kingdom. E-mail: wellst{at}cardiff.ac.uk.

The peptide hormone ghrelin binds to the GH secretagogue receptor (GHS-R), stimulates GH secretion, and promotes adipogenesis. However, continuous GHS infusion does not stimulate skeletal growth and is associated with desensitization to further GH secretagogue treatment. In this study, 7-d intermittent (i.e. every 3 h) infusion of ghrelin, or the GH secretagogue, GH-releasing peptide-6, in the moderately GH- deficient transgenic growth-retarded rat, augmented GH secretion, leading to a sustained acceleration in skeletal growth. In contrast, continuous infusion of ghrelin, or GH-releasing peptide-6, suppressed the amplitude of spontaneous GH secretory episodes and produced only a transient increase in body weight gain. The reduction in GH secretion seen with continuous GHS-R activation was not associated with a desensitization of the pituitary to GH-releasing factor or to down-regulation of hypothalamic GHS-R mRNA expression. Continuous ghrelin treatment elicited an increase in somatostatin mRNA expression in the periventricular nuclei. Thus, exposure to continuously elevated circulating ghrelin may be responsible for the suppression of GH secretion reported in rats after prolonged starvation.

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