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Gene Transcription of Receptors for Growth Hormone-Releasing Peptide and Somatostatin in Human Pituitary Adenomas¹

Medical Department M, Aarhus Kommunehospital, Aarhus University Hospital (S.N., S.M., J.W., J.O.L.J.); Laboratory for Molecular Pathology, Aarhus Kommunehospital, Aarhus University Hospital (L.M.R.); Research Laboratory for Biochemical Pathology, Aarhus Kommunehospital, Aarhus University Hospital (T.L.); Department of Neurosurgery, Aarhus Kommunehospital, Aarhus University Hospital (J.A.), DK-8000 Aarhus C, Denmark

Address correspondence and requests for reprints to: Steen Nielsen MD, Medical Department M (Diabetes and Endocrinology), Aarhus Kommunehospital, DK-8000 Aarhus C, Denmark. E-mail: stn{at}afdm.aau.dk

Growth hormone (GH)-releasing peptides (GHRP) or secretagogs (GHS) constitute a family of synthetic compounds with potent and specific GH releasing activity. The receptor (GHS-R) has recently been cloned even though the endogenous ligand remains to be identified. GHRPs act both at the hypothalamic and the pituitary level through mechanisms involving amplification of GH-releasing hormone activity and functional somatostatin antagonism. In the present study we examined the co-expression of messenger RNA (mRNA) for GHS-R and all 5 somatostatin receptor subtypes (sstr 1–5) in 28 human pituitary tumors by RT-PCR. GHS-R transcription was detected in 11 out of 12 somatotroph adenomas and in 2 out of 2 prolactinomas, whereas GHS-R expression was detected in only 2 out of 14 clinically nonfunctioning adenomas (NFPA), and no expression was seen in the only ACTH secreting adenoma. Almost all tumors expressed sstr 2 mRNA (n = 24), whereas only 1 tumor expressed sstr 4 mRNA. The expression of sstr 3 mRNA was inversely associated with GHS-R expression (P < 0.001), which could be attributed to a high prevalence of sstr 3 expression in NFPA.

This study suggests that GHS-R expression is predominantly observed in somatotroph adenomas and much less so in NFPA. Moreover, the presence of a distinct pattern of somatostatin receptor subtype co-expression is suggested, which may provide a molecular basis for the complex interaction between GHRPs and somatostatin.

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