11 research outputs found
Relationship Between Growth and Plasma Concentrations of Ghrelin and Growth Hormone in Juvenile Beagle Dogs
Acute ghrelin response to intravenous dexamethasone administration in idiopathic short stature or isolated idiopathic growth hormone-deficient children
Pattern-Dependent Suppression of Growth Hormone (GH) Pulsatility by Ghrelin and GH-Releasing Peptide-6 in Moderately GH-Deficient Rats
A Decrease in the Dose of Pegvisomant was Needed for the Treatment of Acromegaly after Adrenalectomy in a Patient with Coexisting Preclinical Cushing's Syndrome
Bofu-Tsu-Shosan, an Oriental Herbal Medicine, Exerts a Combinatorial Favorable Metabolic Modulation Including Antihypertensive Effect on a Mouse Model of Human Metabolic Disorders with Visceral Obesity
Obese Subjects Respond to the Stimulatory Effect of the Ghrelin Agonist Growth Hormone-Releasing Peptide-2 on Food Intake*
Central and Peripheral Administration of Secretin Inhibits Food Intake in Mice through the Activation of the Melanocortin System
Secretin (Sct) is released into the circulation postprandially from the duodenal S-cells. The major functions of Sct originated from the gastrointestinal system are to delay gastric emptying, stimulate fluid secretion from pancreas and liver, and hence optimize the digestion process. In recent years, Sct and its receptor (Sctr) have been identified in discrete nuclei of the hypothalamus, including the paraventricular nucleus (PVN) and the arcuate nucleus (Arc). These nuclei are the primary brain sites that are engaged in regulating body energy homeostasis, thus providing anatomical evidence to support a functional role of Sct in appetite control. In this study, the effect of Sct on feeding behavior was investigated using wild-type (wt), Sct−/−, and secretin receptor-deficient (Sctr−/−) mice. We found that both central and peripheral administration of Sct could induce Fos expression in the PVN and Arc, suggesting the activation of hypothalamic feeding centers by this peptide. Consistent with this notion, Sct was found to increase thyrotropin-releasing hormone and melanocortin-4 receptor (Mc4r) transcripts in the PVN, and augment proopiomelanocortin, but reduces agouti-related protein mRNA expression in the Arc. Injection of Sct was able to suppress food intake in wt mice, but not in Sctr−/− mice, and that this effect was abolished upon pretreatment with SHU9119, an antagonist for Mc4r. In summary, our data suggest for the first time that Sct is an anorectic peptide, and that this function is mediated by the melanocortin system