[HTML][HTML] Raising Awareness: The Need to Promote Allocation of Pancreata from Rare Non-Diabetic Donors with Pancreatic Islet Autoimmunity to Type 1 Diabetes …

GW Burke III, AL Posgai, CH Wasserfall… - American journal of …, 2017 - ncbi.nlm.nih.gov
GW Burke III, AL Posgai, CH Wasserfall, MA Atkinson, A Pugliese
American journal of transplantation: official journal of the American …, 2017ncbi.nlm.nih.gov
We would like to engage the transplant community and ask support for research about the
causes of type 1 diabetes (T1D): we discuss here the critical need to facilitate allocation to
research of pancreata from those rare organ donors with recent onset T1D or prediabetes.
First, it is key to recognize that our knowledge of T1D pathogenesis and etiological factors is
severely limited by scarce access to the pancreas of patients. To address this shortcoming,
the JDRF supported the institution of the Network for the Pancreatic Organ Donors with …
We would like to engage the transplant community and ask support for research about the causes of type 1 diabetes (T1D): we discuss here the critical need to facilitate allocation to research of pancreata from those rare organ donors with recent onset T1D or prediabetes.
First, it is key to recognize that our knowledge of T1D pathogenesis and etiological factors is severely limited by scarce access to the pancreas of patients. To address this shortcoming, the JDRF supported the institution of the Network for the Pancreatic Organ Donors with Diabetes (nPOD; www. JDRFnPOD. org). Working with US Organ Procurement Organizations (OPOs) nPOD has recovered pancreata from over 100 organ donors with T1D since 2007. nPOD promotes collaborative research by providing specimens to qualified investigators, worldwide, as well as scientific leadership and coordination (1). Many novel discoveries have been made through the study of nPOD pancreata (1) about key elements of the autoimmune pathogenesis and additional mechanisms of disease, including chronic inflammation associated with beta cell stress and dysfunction, alterations of key extracellular matrix components in the islets, alteration of the exocrine tissue, and more. Growing evidence shows that the disease is more chronic than previously thought, as pathological signs and insulin-positive beta cells persist for many years, sometimes decades, after clinical diagnosis.
ncbi.nlm.nih.gov