Table of Contents
ISRN Endocrinology
Volume 2012, Article ID 834359, 6 pages
Research Article

Stanniocalcin-1 Co-Localizes with Insulin in the Pancreatic Islets

Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada N6A 5C1

Received 2 August 2012; Accepted 9 September 2012

Academic Editors: A. De Bellis and D. G. Romero

Copyright © 2012 Deenaz Zaidi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The polypeptide hormone stanniocalcin-1 (STC-1) is widely expressed in mammals and signals both locally and systemically. In many tissues STC-1 ligand is sequestered by target cell organelles (mitochondria, nuclei, and cholesterol lipid droplets) to exert diverse biological effects. Most notably, STC-1 serves as an uncoupler of oxidative phosphorylation in liver, muscle, and kidney mitochondria. The present paper describes the identification of STC-1 receptors in mouse pancreatic β cells and the discovery that the ligand co-localizes with insulin in pancreatic β cells. In situ hybridization (ISH) analysis subsequently revealed that pancreatic β cells were the source of the ligand. Intriguingly however, all ISH signal was localized over putative islet cell nuclei as opposed to the cell cytoplasm. Real-time qPCR and agarose gel electrophoresis revealed that the STC-1 amplicon generated from islet cell total RNA was the same size as that from kidney. However, relative levels of STC-1 gene expression were >100-fold lower in islets than those in kidney tissue. Collectively, these findings are indicative of a local STC-1 signalling pathway in pancreatic β cells. The role of STC-1 in this context remains to be established, but it could very well entail the regulation of β cell mitochondria membrane potential which is an integral aspect of regulated insulin release. Interestingly, STC-1 immunoreactivity was not evident in embryonic pancreatic islets, suggesting that ligand synthesis may only commence postnatally.