BETA CELL FUNCTION USING THE HYPERGLYCEMIC CLAMP AFTER HEMIPANCREATECTOMY

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The aim of this project is to study the mechanisms of Beta-cell adaptation to stress in baboon n pancreatic islets. The mechanisms of Beta-cell adaptation to an increased secretory demand have not been studied in Non Human Primates (NHP). Unlike in humans, measurements of changes in islet morphology and turnover can be done prospectively in NHPs. Although islet amyloid deposition is the most typical feature of NHP and human T2DM, our knowledge on amyloid biology and pathophysiology is almost completely related on studies performed on rodents. Another valuable model for the study of amyloidosis and B-cell failure is provided by cultured and transplanted human islets, which rapidly develop amyloidosis, B-cell degeneration and dysfunction. No effective treatments capable to prevent or decrease islet amyloid deposition have yet come to fruition. This project is intended to contribute at filling some of these gaps.