OnLine Journal of Biological Sciences

Effect of Alloxan-Diabetes on Gastrin-Releasing Peptide (GRP) Immunoreactivity in the Gastrointestinal Tract, of Sprague Dawley Rats and How This May Affect Some of the Diabetic Complications

Edward O. Uche-Nwachi and Camille V. Mitchell

DOI : 10.3844/ojbsci.2007.3.7

OnLine Journal of Biological Sciences

Volume 7, Issue 1

Pages 3-7


Gastrin-releasing peptide (GRP) is the mammalian analogue of bombesin. Both neuroendocrine peptides have similar distribution, functions and immunoreactivity. The immunoreactivity for GRP has been demonstrated in the esophagus, stomach and small intestine. This peptide is reported to have various biological and pharmacological properties, which include the release of gastrointestinal hormones, control of satiety, gastrointestinal motility and stimulation of cellular proliferation which results in wound healing. It is also implicated in the proliferation of many gastrointestinal (GI), renal and prostatic tumours. Transient increase in GRP synthesis in the brain and serum concentration, which was later followed by decreased serum concentration, has been reported in hyperglycemic states. The aim of this investigation was to determine the effect of hyperglycemia on GRP secreting neurons in the sub mucosa of the GIT and how this may affect some of the GI complications of diabetes. Result showed decreased immunoreactivity to GRP in the sub mucosal neurons of the stomach and small intestine in alloxan-diabetic Sprague Dawley rats. We conclude that this could contribute to the hyperglycemia-induced GRP decrease in diabetes. This could contribute to reduced peristalsis, with resultant constipation in diabetics. It is also possible that this may also contribute to poor wound healing in diabetics.


© 2007 Edward O. Uche-Nwachi and Camille V. Mitchell. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.