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Department of Medicine and Clinical Science (K.T., H.A., N.K., H.I., A.Y., M.H., K.M., Y.K., Y.O., K.H., T.A., K.N.), Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan; Clinical Research Institute Center for Endocrine and Metabolic Diseases (T.U., A.S.), Kyoto National Hospital, Kyoto 612-8555, Japan; and Department of Biochemistry, National Cardiovascular Center Research Institute (M.K., K.K.), Osaka 565-8565, Japan
Abstract
Ghrelin is a recently identified endogenous ligand for the GH secretagogue receptor and is involved in a novel system for regulating GH release. However, little is known about its GH-releasing activity and other endocrine effects in humans. To address this issue, we studied the GH, ACTH, cortisol, PRL, LH, FSH, and TSH responses to synthetic human ghrelin. In four normal male adults (28–37 yr), iv ghrelin administration released GH in a dose-dependent manner and 0.2, 1.0, and 5.0 µg/kg ghrelin produced 43.3 ± 6.0, 81.5 ± 12.7, and 107.0 ± 10.7 ng/mL of the GH peak values at 30 min, respectively. ACTH, cortisol, and PRL levels were also elevated after ghrelin injection, while the lowest dose (0.2 µg/kg) resulted in only minimum peak values of these hormones (22.8 ± 3.0 pg/mL, 9.4 ± 1.9 µg/dL, and 4.6 ± 0.6 ng/mL, respectively). There were no significant changes in LH, FSH, or TSH levels. This is the first study showing evidence that ghrelin strongly stimulates GH release in humans.
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J. Iqbal, Y. Kurose, B. Canny, and I. J. Clarke Effects of Central Infusion of Ghrelin on Food Intake and Plasma Levels of Growth Hormone, Luteinizing Hormone, Prolactin, and Cortisol Secretion in Sheep Endocrinology, January 1, 2006; 147(1): 510 - 519. [Abstract] [Full Text] [PDF]
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M. Misra, K. K. Miller, V. Stewart, E. Hunter, K. Kuo, D. B. Herzog, and A. Klibanski Ghrelin and Bone Metabolism in Adolescent Girls with Anorexia Nervosa and Healthy Adolescents J. Clin. Endocrinol. Metab., September 1, 2005; 90(9): 5082 - 5087. [Abstract] [Full Text] [PDF]
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H. Ariyasu, K. Takaya, H. Iwakura, H. Hosoda, T. Akamizu, Y. Arai, K. Kangawa, and K. Nakao Transgenic Mice Overexpressing Des-Acyl Ghrelin Show Small Phenotype Endocrinology, January 1, 2005; 146(1): 355 - 364. [Abstract] [Full Text] [PDF]
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