The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Ghrelin stimulation of growth hormone release and appetite is mediated through the growth hormone secretagogue receptor
Open accessAbstract
Synthetic agonists of the growth hormone secretagogue receptor (GHSR) rejuvenate the pulsatile pattern of GH-release in the elderly, and increase lean but not fat mass in obese subjects. Screening of tissue extracts in a cell line engineered to overexpress the GHSR led to the identification of a natural agonist called ghrelin. Paradoxically, this hormone was linked to obesity. However, it had not been directly shown that the GHSR is a physiologically relevant ghrelin receptor. Furthermore, ghrelin's structure is significantly different from the synthetic agonist (MK-0677) used to expression-clone the GHSR. To address whether the GHSR mediates ghrelin's stimulatory effects on GH release and appetite, we generated Ghsr-null mice. In contrast to wild-type mice, acute treatment of Ghsr-null mice with ghrelin stimulated neither GH release nor food intake, showing that the GHSR is a biologically relevant ghrelin receptor. Nevertheless,Ghsr-null mice are not dwarfs; their appetite and body composition are comparable to that of wild-type littermates. Furthermore, in contrast to suggestions that ghrelin regulates leptin and insulin secretion, fasting-induced changes in serum levels of leptin and insulin are identical in wild-type and null mice. Serum insulin-like growth factor 1 levels and body weights of mature Ghsr-null mice are modestly reduced compared to wild-type littermates, which is consistent with ghrelin's property as an amplifier of GH pulsatility and its speculated role in establishing an insulin-like growth factor 1 set-point for maintaining anabolic metabolism. Our results suggest that chronic treatment with ghrelin antagonists will have little effect on growth or appetite.
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Cites
Ghrelin is a growth-hormone-releasing acylated peptide from stomach
Kojima, M., Hosoda, H., Date, Y., Nakazato, M., Matsuo, H., & Kangawa, K. (1999) · Nature · doi:10.1038/45230 · Cited by 8,479
Ghrelin induces adiposity in rodents
Tschöp, M., Smiley, D. L., & Heiman, M. L. (2000) · Nature · doi:10.1038/35038090 · Cited by 3,949
A role for ghrelin in the central regulation of feeding
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Plasma Ghrelin Levels after Diet-Induced Weight Loss or Gastric Bypass Surgery
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Leptin Inhibits Bone Formation through a Hypothalamic Relay
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A Receptor in Pituitary and Hypothalamus That Functions in Growth Hormone Release
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Self-citationThe Tissue Distribution of the mRNA of Ghrelin and Subtypes of Its Receptor, GHS-R, in Humans
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Self-citationGhrelin Causes Hyperphagia and Obesity in Rats
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Cited by
Watterson, K. R., Bestow, D., Gallagher, J., Hamilton, D. L., Ashford, F. B., Meakin, P. J., & Ashford, M. L. J. (2013) · Neurosignals · doi:10.1159/000334144 · Cited by 3,389
Ghrelin: Structure and Function
Kojima, M., & Kangawa, K. (2005) · Physiological Reviews · doi:10.1152/physrev.00012.2004 · Cited by 2,810
The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review
Klok, M. D., Jakobsdottir, S., & Drent, M. L. (2007) · Obesity Reviews · doi:10.1111/j.1467-789x.2006.00270.x · Cited by 1,442
The Human Obesity Gene Map: The 2005 Update
Rankinen, T., Zuberi, A., Chagnon, Y. C., Weisnagel, S. J., Argyropoulos, G., Walts, B., Pérusse, L., & Bouchard, C. (2006) · Obesity · doi:10.1038/oby.2006.71 · Cited by 1,119
Expression of ghrelin receptor mRNA in the rat and the mouse brain
Zigman, J. M., Jones, J. E., Lee, C. E., Saper, C. B., & Elmquist, J. K. (2006) · The Journal of Comparative Neurology · doi:10.1002/cne.20823 · Cited by 1,074
Metadata
- Authors
- Sun, Y., Wang, P., Zheng, H., & Smith, R. G.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2004-03-18
- Volume
- 101
- Issue
- 13
- Pages
- 4679-4684
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2144489715
- Cited by
- 745
- References
- 33
- FWCI
- 16.91
- Type
- journal article
- Language
- en
- Open access
- green
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