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Ghrelin-induced feeding is dependent on nitric oxide
F Spencer Gaskin1, Susan A Farr, William A Banks
1Department of Internal Medicine, Geriatric Research Education and Clinical Center, VA Medical Center, Division of Geriatric Medicine, St. Louis University School of Medicine, 915 N. Grand Blvd., St. Louis, MO 63106, USA.
Peptides
|September 2, 2003
Summary
Ghrelin, a gastric peptide, increases food intake. This effect is dependent on nitric oxide (NO), a molecule that regulates feeding behaviors.
Area of Science:
- Neuroendocrinology
- Gastroenterology
- Physiology
Background:
- Ghrelin is a gastric peptide with orexigenic (appetite-stimulating) properties.
- Ghrelin acts as the endogenous ligand for the growth hormone secretagogue receptor.
- Nitric oxide (NO) is known to mediate feeding responses induced by various neuropeptides.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in mediating the orexigenic effects of ghrelin.
- To determine if ghrelin-induced feeding is dependent on NO signaling pathways.
Main Methods:
- Administered ghrelin intracerebroventricularly to satiated mice to assess food intake.
- Utilized N(omega)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, to block NO production.
- Measured nitric oxide synthase levels in the hypothalamus following ghrelin administration.
Main Results:
- Intracerebroventricular ghrelin administration significantly increased food intake in satiated mice.
- A subthreshold dose of L-NAME significantly blocked the ghrelin-induced increase in food intake.
- Ghrelin administration led to increased nitric oxide synthase levels in the hypothalamus.
Conclusions:
- Ghrelin's orexigenic effects are mediated by nitric oxide (NO).
- Nitric oxide acts as a central regulator of food consumption, particularly in response to ghrelin.
- These findings elucidate a key signaling pathway involved in appetite regulation.