Journal of Capital Medical University ›› 2005, Vol. 26 ›› Issue (3): 333-335.

Previous Articles     Next Articles

Effects of Severe Acute Pancreatitis on the Level of Serum Insulin and Glucagon in Rats

Liu Dongbin, Sun Jiabang, Li Fei, Zhang Sunwen, Sun Haichen, Cui Yeqing, Liu Shuang, Liu Dachuan   

  1. Department of General Surgery, Xuanwu Hospital, Capital University of Medical Sciences
  • Received:2004-12-20 Revised:1900-01-01 Online:2005-06-24 Published:2005-06-24

Abstract:

Objective To study the effects of severe acute pancreatitis on the level of serum insulin and glucagon in rats. Methods SAP model was produced by retrograde injection of 3.5% sodium taurocholate into the cannulated biliopancreatic duct, and rats were sacrificed at 6, 24, 48, 72 h after induction of pancreatitis. The pancreatic tissue specimens were collected to assess the pathological score of exocrine part in terms of tissue damage and Bcl-2 expression was observed with immunohistochemical examination. Prior to sacrifice, blood samples in 6, 24, 48, 72 h were taken from the inferior vena cava to measure serum insulin and glucagons with radioimmunoassay (RIA). Results Tissue damage got worse with time passing and maximized at 24 h after SAP model established. With the development of disorder, the pancreas presented necrosis, hemorrhage and severe leukocytes infiltration. The serum insulin level markedly decreased at 24, 48, 72 h, and the level of glucagon significantly increased at 6, 24, 48, 72 h compared with the experimental control group and normal control group. The differences were significant statistically. Immunohistochemistry examination showed that the Bcl-2 expressed in islets of SAP rats after 6 h, however disappeared after 24 h. Conclusion Severe acute pancreatitis impairs both the pancreatic exocrine and endocrine functions. On the other hand, the Bcl-2 expression in immunohistological examination indicated that there might be a protective mechanism against the endocrine dysfunction in SAP, in which Bcl-2 was involved.

Key words: acute pancreatitis, animal model, insulin, glucagon

CLC Number: