title: The role of noggin in regulation of high glucose-induced apoptosis and insulin secretion in INS-1 rat beta cells.
abstract: OBJECTIVE
  The purpose of this study was to investigate the effects of Noggin on high glucose-induced apoptosis and insulin secretion in pancreatic beta cells.
  
  
  METHODS
  Different concentrations of glucose were used to examine their effects on INS-1 rat beta cells in vitro. When specific siRNA targeting Noggin and recombinant Noggin were added, apoptosis and insulin secretion were measured, respectively to determine their effects in INS-1 cells.
  
  
  RESULTS
  Glucose stimulated the expression of Noggin in a dose-dependent manner. Knockdown of Noggin further increased apoptosis and reduced insulin secretion when INS-1 cells were exposed to high glucose. Conversely, administration of recombinant Noggin significantly reduced apoptotic cell number, and promoted insulin secretion. Finally, treatment with inhibitor of Smad phosphorylation exerted similar effects on cell apoptosis and insulin production to Noggin administration in glucose-treated INS-1 cells.
  
  
  CONCLUSIONS
  Our findings indicate that Noggin inhibits apoptosis and promotes insulin secretion in pancreatic beta cells through the inhibition of Smad signaling. Gene therapy of delivering Noggin may facilitate the treatment for patients with type 2 diabetes mellitus.
authors.affiliation: Department of Endocrinology, the Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China, 161000.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of General Surgery, the Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China, 161000.
authors.forename: Zhanjiang
authors.initials: Z
authors.lastname: Yu
authors.affiliation: Department of Anatomy, Qiqihar Medical University, Qiqihar, Heilongjiang, China, 161006.
authors.forename: Fengchun
authors.initials: F
authors.lastname: Deng
keywords: Apoptosis; Insulin; Noggin; Pancreatic beta cell; Smad; Type 2 diabetes mellitus