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Endocrinology Vol. 140, No. 8 3790-3796
Copyright © 1999 by The Endocrine Society

ARTICLES

Colocalization of Somatostatin Receptor sst5 and Insulin in Rat Pancreatic ß-Cells1

Sudha Warrier Mitra, Éva Mezey, Bela Hunyady, LaShawn Chamberlain, Edward Hayes, Forrest Foor, Yining Wang, Agnes Schonbrunn and James M. Schaeffer

Department of Endocrinology and Chemical Biology, Merck Research Laboratories, Merck & Co., Inc. (S.W.M., L.C., E.H., F.F., J.M.S.), Rahway, New Jersey 07065; the National Institute of Neurological Disorders and Stroke, Basic Neuroscience Program, National Institutes of Health (E.M., B.H.), Bethesda, Maryland 20892; and the Department of Integrative Biology and Pharmacology, University of Texas Health Sciences Center (Y.W., A.S.), Houston, Texas 77030

Address all correspondence and requests for reprints to: Dr. Sudha Warrier Mitra, Department of Endocrinology and Chemical Biology, Merck Research Laboratories, R80Y-310, P.O. Box 2000, Rahway, New Jersey 07065. E-mail: sudha_mitra{at}merck.com

Somatostatin, also known as somatotropin release-inhibiting factor (SRIF), is secreted by pancreatic {delta}-cells and inhibits the secretion of both insulin and glucagon. SRIF initiates its actions by binding to a family of six G protein-coupled receptors (sst1, -2A, -2B, -3, -4, and -5) encoded by five genes. Messenger RNA for both sst2 and sst5 have been reported in the rat pancreas, and the sst2A receptor protein has been localized to rat pancreatic {alpha} and pancreatic polypeptide-secreting cells in the islets as well as to pancreatic acinar cells. In this study we have used double immunostaining to show that the sst5 protein is expressed exclusively in the ß-cells of rat pancreatic islets and localizes with insulin-secreting {alpha}-cells. The sst5 receptor is not colocalized with sst2A. Thus, in the rat SRIF inhibits pancreatic insulin and glucagon secretion via different sst receptor subtypes.




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