title: Alteration of the pancreatic endocrine component in the early stage of acute necrotic pancreatitis in rats.
abstract: OBJECTIVE
  To investigate alterations of the pancreatic endocrine component in the early stage of acute necrotic pancreatitis (ANP) in rats.
  
  
  METHODS
  Thirty-six Sprague-Dawley rats were randomly allocated to two groups: ANP group (n = 18) and sham-operated (control) group (n = 18). ANP was induced by retrograde injection of 4% sodium deoxycholate (40 mg/kg, 0.1 mL/min) into the biliopancreatic duct and the severity of pancreatitis induced was assessed by histopathological examination and level of plasma amylase. The pancreatic endocrine function was assessed by measuring the levels of plasma glucose and insulin and by measuring the insulin content in pancreatic beta cells by immunofluorescence and immunocytochemistry.
  
  
  RESULTS
  Five hours after operation, the pancreas of rats in the ANP group showed pathological changes with edema, hemorrhage, fatty necrosis, acinar destruction and leukocyte infiltration in the exocrine portion of the pancreas. Plasma amylase activity increased significantly (P < 0.01) and bloody ascites appeared in the abdominal cavity. Nevertheless the endocrine islets appeared normal and the beta cells contained intensive labeling of insulin. Levels of glucose and insulin in plasma increased significantly. In the ANP group, 5 h after operation the plasma level of glucose was 8.18 +/- 2.26 mmol/L vs 6.39 +/- 1.26 mmol/L, and of insulin was 23.27 +/- 3.50 MIU/L vs 18.40 +/- 3.98 MIU/L. In the control group, 5 h after operation the plasma level of glucose was 9.39 +/- 0.62 mmol/L vs 5.89 +/- 0.62 mmol/L, and of insulin was 26.28 +/- 4.77 MIU/L vs 12.89 +/- 2.05 MIU/L; there was no significant difference between these two groups (P > 0.05). After a bolus injection of glucose, however, a much higher level of insulin was found in the control group (35.30 +/- 5.05 MIU/L) than that in the ANP group (23.91 +/- 4.62 MIU/L, P < 0.05).
  
  
  CONCLUSIONS
  There may be an impaired ability of insulin release in response to glucose stimulation in the early stage of ANP, although the morphology of the pancreatic endocrine component remains intact.
authors.affiliation: Department of Pathophysiology, Medical School of Tongji University, Shanghai, China. liyongyu@mail.tongji.edu.cn
authors.forename: Yong Yu
authors.initials: YY
authors.lastname: Li
authors.forename: Guo Ying
authors.initials: GY
authors.lastname: Zhu
authors.forename: Yong Xin
authors.initials: YX
authors.lastname: Gao
authors.forename: Zhi Yong
authors.initials: ZY
authors.lastname: Yang
authors.forename: Zhu Yi
authors.initials: ZY
authors.lastname: Wang
mesh_terms: D000681:Amylases / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D003840:Deoxycholic Acid; D004195:Disease Models, Animal; D005260:Female; D007328:Insulin / Q000097:blood*; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology; D008297:Male; D010179:Pancreas / Q000473:pathology / Q000503:physiopathology*; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D001786:Blood Glucose; D007328:Insulin; D003840:Deoxycholic Acid; D000681:Amylases