title: Effects of ORP150 on appearance and function of pancreatic beta cells following acute necrotizing pancreatitis.
abstract: Pancreatic beta cells produce and release insulin, which decreases the blood glucose level. Endoplasmic reticulum stress caused pancreatic beta cell dysfunction and death in acute necrotizing pancreatitis (ANP). The 150kD oxygen-regulated protein (ORP150) took part in the process of endoplasmic reticulum stress. This study investigated the effect of ORP150 on appearance and function of pancreatic beta cells in ANP. Acute necrotizing pancreatitis relied on retrograde infusion of 5% sodium taurocholate into the bile-pancreatic duct. The severity of ANP was estimated by serum amylase, secretory phospholipase A(2,) and pancreatic histopathology. The changes in appearance and function of pancreatic beta cells were detected by light and electron microscopy and the levels of serum glucose, insulin, and C-peptide. ORP150 expression was studied using western blot and immunohistochemisty assay. The expression of ORP150 mainly appeared on pancreatic beta cells and decreased gradually during the pathogenesis of ANP. The results of light and electron microscopy indicated pancreatic beta cell dysfunction and death, concomitant with elevation of serum glucose, insulin, and C-peptide in ANP. These results imply a probable role of ORP150 in the changes in appearance and function of pancreatic beta cells following acute necrotizing pancreatitis, through the pathway of endoplasmic reticulum stress.
authors.affiliation: Department of General Surgery, Renmin Hospital of Wuhan University, 238 Jiefang Road, 430060, Hubei Province, People's Republic of China.
authors.forename: Wen-Hong
authors.initials: WH
authors.lastname: Deng
authors.forename: Chen
authors.initials: C
authors.lastname: Chen
authors.forename: Wei-Xing
authors.initials: WX
authors.lastname: Wang
authors.forename: Jia
authors.initials: J
authors.lastname: Yu
authors.forename: Jin-You
authors.initials: JY
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Liu
mesh_terms: D000681:Amylases / Q000097:blood; D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D002096:C-Peptide / Q000097:blood; D004195:Disease Models, Animal; D004721:Endoplasmic Reticulum / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins; D007150:Immunohistochemistry; D007328:Insulin / Q000097:blood; D050417:Insulin-Secreting Cells / Q000378:metabolism* / Q000648:ultrastructure; D008297:Male; D046529:Microscopy, Electron, Transmission; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D054497:Phospholipases A2, Secretory / Q000097:blood; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013656:Taurocholic Acid; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D018840:HSP70 Heat-Shock Proteins; D007328:Insulin; D011506:Proteins; C050087:oxygen-regulated proteins; D013656:Taurocholic Acid; D054497:Phospholipases A2, Secretory; D000681:Amylases