Central Administration of Aminoprocalcitonin Inhibits Food Intake and Stimulates the Hypothalamic-Pituitary-Adrenal Axis in Rats via the Corticotrophin-Releasing Factor System
| Autor: | Francisco J. Miñano, Rosario Maldonado, A.M. García-Martínez, Eva Tavares |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
endocrine system
medicine.medical_specialty Endocrinology Diabetes and Metabolism Population Energy homeostasis Cellular and Molecular Neuroscience chemistry.chemical_compound Endocrinology Corticosterone Internal medicine parasitic diseases medicine education education.field_of_study Glial fibrillary acidic protein biology Endocrine and Autonomic Systems digestive oral and skin physiology medicine.anatomical_structure nervous system chemistry Hypothalamus biology.protein NeuN hormones hormone substitutes and hormone antagonists Hypothalamic–pituitary–adrenal axis Astrocyte |
| Zdroj: | Journal of Neuroendocrinology. 24:1040-1054 |
| ISSN: | 0953-8194 |
| DOI: | 10.1111/j.1365-2826.2012.02308.x |
| Popis: | Aminoprocalcitonin (N-PCT), a neuroendocrine peptide derived from procalcitonin, reduces food intake and body weight when administered centrally in rats. We have recently shown that N-PCT is expressed in brain areas known to be involved in energy homeostasis, including the paraventricular nucleus (PVN) of the hypothalamus, which contains a prominent population of corticotrophin-releasing factor (CRF)-synthesising neurones. CRF plays a pivotal role in the regulation of the hypothalamic-pituitary adrenal (HPA) axis and food intake. However, little is known about functional interactions of N-PCT and CRF. In the present study, we found endogenous N-PCT protein in the rat PVN. We also showed N-PCT immunoreactivity in PVN co-localised with NeuN, a neuronal marker, or glial fibrillary acidic protein, an astrocyte marker. Double staining immunohistochemistry revealed that N-PCT co-localised with CRF in parvocellular neurones of the PVN. Intracerebroventricular N-PCT administration increased CRF mRNA and content in the hypothalamus, suggesting that N-PCT stimulates the HPA axis and suppresses food intake and body weight via CRF-dependent pathways. In keeping with this, i.c.v. co-injection of D-Phe-CRF(12-41), a CRF receptor antagonist, significantly attenuated N-PCT-induced reduction in food intake and body weight in a dose-dependent manner. Furthermore, i.c.v. administration of N-PCT increased plasma adrenocorticotrophic hormone and corticosterone concentrations and induced the expression of Fos protein, a marker of neuronal activity, in parvocellular CRF neurones. These data collectively support the hypothesis that N-PCT inhibits food intake and body weight and stimulates the HPA axis via CRF-mediated pathways. |
| Databáze: | OpenAIRE |
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