INTRODUCTION: Impairment in pancreatic endocrine function is believed to play an important role in the development of glucose intolerance in acute pancreatitis. AIM: To investigate the functional aspects of endocrine cells in acute pancreatitis and the expression of glucose transporter (GLUT) 2 in the pancreatitis islet. METHODOLOGY: A mild form of acute pancreatitis was induced in rats by an injection of a sodium taurocholate solution via a cannulated biliopancreatic duct. Isolated islets were stimulated by glucose, and insulin secretion was analyzed by radioimmunoassay. Immunohistochemical detection of GLUT2 with use of a specific antibody was attempted to determine GLUT2 expression in pancreatic islets. RESULTS: A marked elevation of glucose levels observed in the current rat pancreatitis model confirmed that glucose intolerance can occur even in a mild form of pancreatitis. The architecture of the islets, however, remained intact despite marked inflammatory changes in the neighboring exocrine region. Insulin secretion studies revealed that the ability of islets to secrete insulin in response to glucose was markedly reduced in pancreatitis islets. GLUT2 immunoreactivity in endocrine cells was found to be intact in pancreatitis islets. CONCLUSION: The amount of insulin released from isolated islets following glucose stimulation is reduced in acute edematous pancreatitis, although pancreatic islets remain histologically intact. On the basis of the present findings, it appears that although the mechanisms responsible for this functional deficiency remain to be determined, the decrease in insulin secretion is possibly caused by impairment of some pancreatic B-cell functions rather than GLUT2-mediated glucose transportation.
INTRODUCTION: Impairment in pancreatic endocrine function is believed to play an important role in the development of glucose intolerance in acute pancreatitis. AIM: To investigate the functional aspects of endocrine cells in acute pancreatitis and the expression of glucose transporter (GLUT) 2 in the pancreatitis islet. METHODOLOGY: A mild form of acute pancreatitis was induced in rats by an injection of a sodium taurocholate solution via a cannulated biliopancreatic duct. Isolated islets were stimulated by glucose, and insulin secretion was analyzed by radioimmunoassay. Immunohistochemical detection of GLUT2 with use of a specific antibody was attempted to determine GLUT2 expression in pancreatic islets. RESULTS: A marked elevation of glucose levels observed in the current ratpancreatitis model confirmed that glucose intolerance can occur even in a mild form of pancreatitis. The architecture of the islets, however, remained intact despite marked inflammatory changes in the neighboring exocrine region. Insulin secretion studies revealed that the ability of islets to secrete insulin in response to glucose was markedly reduced in pancreatitis islets. GLUT2 immunoreactivity in endocrine cells was found to be intact in pancreatitis islets. CONCLUSION: The amount of insulin released from isolated islets following glucose stimulation is reduced in acute edematous pancreatitis, although pancreatic islets remain histologically intact. On the basis of the present findings, it appears that although the mechanisms responsible for this functional deficiency remain to be determined, the decrease in insulin secretion is possibly caused by impairment of some pancreatic B-cell functions rather than GLUT2-mediated glucose transportation.