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This version published online on May 16, 2006
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-0105
A more recent version of this article appeared on August 1, 2006
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Submitted on January 17, 2006
Accepted on May 5, 2006

The N-terminal Neurotensin Fragment, NT1-11, Inhibits Cortisol Secretion by Human Adrenocortical Cells

Flavie Sicard, Vincent Contesse, Hervé Lefebvre, Djida Ait-Ali, Marjorie Gras, Dorthe Cartier, Annick Decker, Nicolas Chartrel, Youssef Anouar, Hubert Vaudry, and Catherine Delarue*

INSERM U 413, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23) (F.S., V.C., H.L., D.A-A., M.G., D.C., A.D., N.C., Y.A., H.V., C.D), University of Rouen, 76821 Mont-Saint-Aignan, France; and Department of Endocrinology and Metabolic Diseases (H.L.), Centre Hospitalier Universitaire of Rouen, 76031 Rouen, France

* To whom correspondence should be addressed. E-mail: catherine.delarue{at}univ-rouen.fr.

Context: Neurotensin (NT) modulates corticosteroid secretion from mammalian adrenal gland.

Objective: To investigate the possible involvement of NT in the control of cortisol secretion in the human adrenal gland.

Design: In vitro studies on cultured human adrenocortical cells.

Setting: University research laboratory.

Patients: Adrenal explants from patients undergoing expanded nephrectomy for kidney cancer.

Main outcome measure: Cortisol secretion from cultured adrenocortical cells.

Results: NT1-11, the N terminal fragment of NT, dose-dependently inhibited basal and ACTH-stimulated cortisol production by human adrenocortical cells in primary culture. In contrast, NT had no influence on cortisol output at concentrations up to 10-6 M. HPLC and RT-PCR analyses failed to detect any significant amounts of NT and NT mRNA, respectively, in adrenal extracts. Molecular and pharmacological studies were performed to determine the type of NT receptor involved in the corticostatic effect of NT1-11. RT-PCR analysis revealed the expression of NTR3 mRNA but not NTR1 and NTR2 mRNAs in the human adrenal tissue. However, the pharmacological profile of the adrenal NT1-11 receptor was different from that of NTR3 indicating that this receptor type is not involved in the action of NT1-11 on corticosteroidogenesis.

Conclusion: Our results indicate that NT1-11 may act as an endocrine factor to inhibit cortisol secretion through activation of a receptor distinct from the classical NTR1, NTR2 and NTR3.
Key words: adrenal gland • cortisol secretion • NT • NT1-11 • neurotensin receptors






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