Expression of somatostatin receptor mRNAs is regulated in vivo by growth hormone, insulin, and insulin-like growth factor-I in rainbow trout ( Oncorhynchus mykiss)

• Published in: Regulatory peptides Vol. 128; no. 1; pp. 27 - 32
• Main Authors: Slagter, Barton J., Kittilson, Jeffrey, Sheridan, Mark A.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 15.05.2005; Amsterdam Elsevier
• Subjects: Animals; Base Sequence; Biological and medical sciences; Blood Glucose - analysis; DNA Primers; Female; Fundamental and applied biological sciences. Psychology; Growth Hormone - physiology; Insulin - physiology; Insulin-Like Growth Factor I - physiology; Male; Oncorhynchus mykiss; Real-time quantitative PCR; Receptors, Somatostatin - genetics; RNA, Messenger - genetics; Somatostatin receptor expression; Somatostatin receptor subtype 1A; Somatostatin receptor subtype 1B; Somatostatin receptor subtype 2; Vertebrates: endocrinology; Real-time quantitative PCR; Somatostatin receptor subtype 2; Somatostatin receptor subtype 1B; Somatostatin receptor expression; Somatostatin receptor subtype 1A; Pancreatic hormone; Somatostatin receptor; Somatostatin receptor subtype IA; Somatotropin hormone; Insulin like growth factor 1; Oncorhynchus mykiss; Insulin; Polymerase chain reaction; In vivo; Vertebrata; Adenohypophyseal hormone; Pisces; Subtype
• ISSN: 0167-0115; 1873-1686
• DOI: 10.1016/j.regpep.2004.12.014

Somatostatins are a diverse family of peptide hormones that regulate various aspects of growth, development, and metabolism through interactions with numerous somatostatin receptor subtypes (SSTRs) on target tissues. In this study, we used rainbow trout to evaluate the effects of growth hormone (GH), insulin (INS), and insulin-like growth factor-I (IGF-I) on the expression of SSTR 1A, 1B and 2 mRNAs. GH regulated the expression of SSTRs in a subtype- and tissue-specific manner. GH reduced SSTR 1A, 1B, and 2 expression in optic tectum, reduced SSTR 1A and 1B expression in pancreas, reduced SSTR 1A expression in liver, and increased hepatic SSTR 1B expression. INS also regulated SSTR expression in a subtype- and tissue-specific manner. INS reduced SSTR 1B expression in optic tectum, increased SSTR 2 expression in pancreas, and increased SSTR 1B and 2 expression in liver. IGF-I generally decreased the expression of all SSTRs. These data indicate that GH, INS, and IGF-I modulate the expression of SSTRs and suggest that independent mechanisms may serve to regulate the various receptor subtypes.