• IAPP
  • Because it is not possible to evaluate β-cell mass or turnover in vivo in humans, we undertook these studies in the human IAPP transgenic (HIP) rat because it approximates the islet and metabolic phenotype of type 2 diabetes in humans ( 10 - 12 ). (diabetesjournals.org)
  • We have developed a mouse monoclonal antibody against rat/mouse islet amyloid polypeptide (IAPP). (diva-portal.org)
  • Previous immunohistochemical studies of human pancreatic tissue from individuals with non-insulin-dependent diabetes mellitus (NIDDM) have revealed a paradoxical and unexplained lack of IAPP immunoreactivity in beta cells close to amyloid in spite of the presence of IAPP mRNA. (diva-portal.org)
  • In contrast to these findings we show that the newly developed monoclonal IAPP antibody strongly labels such beta cells while islet amyloid deposits which are labelled by polyclonal antisera do not bind the monoclonal antibody. (diva-portal.org)
  • Knowledge of these structural changes that may include abnormal folding or chemical modification of IAPP is probably important for the understanding of the amyloidogenesis and the pathogenesis of the islet lesion in NIDDM. (diva-portal.org)
  • Because all human subjects produce and secrete the amyloidogenic form of IAPP, yet not all develop islet amyloid, some other factors must be involved in islet amyloid formation. (diva-portal.org)
  • In the pancreatic islets from patients with type 2 diabetes and diabetic cat, MAb4A5 labels immunohistochemically cellular IAPP but not IAPP in islet amyloid deposits. (diva-portal.org)
  • In contrast to MAb4A5 polyclonal rabbitiAPP antisera label beta cells close to amyloid only weakly, but label strongly IAPP in its amyloid form. (diva-portal.org)
  • type 2 diabet
  • OBJECTIVE We sought to establish the extent and mechanisms by which sitagliptin and metformin singly and in combination modify islet disease progression in human islet amyloid polypeptide transgenic (HIP) rats, a model for type 2 diabetes. (diabetesjournals.org)
  • The cause of the defect in β-cell mass in type 2 diabetes remains unresolved but is likely attributable, at least in part, to endoplasmic reticulum stress-induced β-cell apoptosis, noted both at autopsy and in isolated islets from people with type 2 diabetes ( 8 , 9 ). (diabetesjournals.org)
  • Our primary objective in the current study was to test the hypothesis that the combination of two potentially synergistic therapies, the dipeptidyl peptidase-4 (DPP-4) inhibitor sitagliptin and hepatic insulin sensitizer metformin, modify progression of islet dysfunction and loss of β-cell mass in type 2 diabetes. (diabetesjournals.org)
  • Islet amyloid is the most common characteristic feature of the islets in type 2 diabetes, being found in up to 90% of diabetic patients at post-mortem. (diva-portal.org)