|ISSN No. 1606-7754 Vol.11 No.1&2 April-August 2003|
Pancreatic peptides, neuropeptides and neurotransmitters in diabetes mellitus: a review
Ernest Adeghate, Abdulsamad Ponery
Department of Anatomy, Faculty of Medicine & Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, UAE
Diabetes mellitus is due to defective secretion and/ or function of insulin. It is a common chronic disease affecting up to 6% of the world population. This prevalence increases to about 24% in the island of Nauru and some Middle Eastern countries. Diabetes mellitus is associated with profound changes in the endocrine pancreas. These changes include a significant decrease in the number of beta cells, the cell type that produces and secretes insulin. A decrease in the number of insulin producing cells is more evident in type I diabetes. The decrease in the number of insulin-secreting cells is associated with a concomitant increase in the number of glucagon, somatostatin and pancreatic-polypeptide producing cells. The increase in glucagon producing cells results in hyperglucagonaemia, which further exacerbates the hyperglycaemia induced by lack of insulin. In addition to the changes in the number and plasma levels of pancreatic hormones, the number of calcitonin-gene-related peptide- and galanin-positive cells in the islet of Langerhans decreases after the onset of diabetes. Pancreatic amino butyric acid is also decreased in diabetes. These abnormal changes in the pattern of distribution of peptides, neuropeptides and neurotransmitters may contribute to the pathogenesis of diabetes mellitus.
Key words: peptides, diabetes mellitus, hormones, neuropeptides, neurotransmitters
Diabetes mellitus is a chronic metabolic disease, which is associated with hyperglycaemia. This hyperglycaemia is a result of defective insulin secretion and/or function. The prolonged hyperglycaemia accompanying diabetes causes tissue damage, which results in degenerative complications in many organs including the kidney, heart, muscles, eye and many other organs.1 These degenerative complications arise partly because of the damage inflicted on the blood vessels. This review examines the pattern of distribution of insulin-, glucagon-, somatostatin- and pancreatic polypeptide-containing cells in the pancreas of streptozotocin (STZ)-induced diabetic rats. In addition, the topographical relation of calcitonin gene-related peptide (CGRP)-, galanin-, neuropeptide Y (NPY)- and g-aminobutyric acid (GABA)-positive cells of the endocrine pancreas and their role in determining the pathogenesis of diabetes mellitus is discussed.