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Endocrinology, doi:10.1210/en.2003-0899
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Endocrinology Vol. 145, No. 1 234-242
Copyright © 2004 by The Endocrine Society

Ghrelin and Des-Octanoyl Ghrelin Promote Adipogenesis Directly in Vivo by a Mechanism Independent of the Type 1a Growth Hormone Secretagogue Receptor

Nichola M. Thompson, Dave A. S. Gill, Rhos Davies, Nigel Loveridge, Pamela A. Houston, Iain C. A. F. Robinson and Timothy Wells

School of Biosciences, Cardiff University, Cardiff, United Kingdom CF10 3US; Medical Research Council Bone Research Group, University of Cambridge, Department of Medicine, Addenbrookes Hospital (N.L.), Cambridge, United Kingdom CB2 2QQ; Department of Neuroendocrinology, Division of Neuroscience and Psychological Medicine, Imperial College London, Hammersmith Hospital (P.A.H.), London, United Kingdom W12 0NN; and Division of Molecular Neuroendocrinology, National Institute for Medical Research (I.C.A.F.R.), London, United Kingdom NW7 1AA

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

Ghrelin promotes fat accumulation, despite potent stimulation of the lipolytic hormone, GH. The function of the major circulating isoform of ghrelin, des-octanoyl ghrelin, is unclear, because it does not activate the GH secretagogue receptor (GHS-R1a) and lacks the endocrine activities of ghrelin. We have now addressed these issues by infusing ghrelin, des-octanoyl ghrelin, or synthetic GHS-R1a agonists into three rat models with moderate, severe, or total GH deficiency. We show that in the context of significant GH secretion, the adipogenic effect of systemic ghrelin infusion is pattern dependent. However, this adipogenic action is not mediated by the pituitary hormones. Using a novel unilateral local infusion strategy, we demonstrate that ghrelin promotes bone marrow adipogenesis in vivo by a direct peripheral action. Surprisingly, this effect was also observed with des-octanoyl ghrelin, whereas a potent synthetic GHS-R1a agonist was ineffective. Thus, these adipogenic effects are mediated by a receptor other than GHS-R1a. This is the first in vivo demonstration of a direct adipogenic effect of des-octanoyl ghrelin, a major circulating form of ghrelin that lacks GH-releasing activity. We suggest that the ratio of ghrelin and des-octanoyl ghrelin production could help regulate the balance between adipogenesis and lipolysis in response to nutritional status.




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