Oral application of a periodontal pathogen impacts SerpinE1 expression and pancreatic islet architecture in prediabetes

摘要

Background and ObjectivesEpidemiological studies suggest a close association between periodontitis and prediabetes/insulin resistance but whether periodontitis causes prediabetes in humans is not known. Using various animal models, we have recently established that periodontitis can be an initiator of prediabetes which is characterized by glucose intolerance, hyperinsulinemia, and insulin resistance. In addition, our in vitro studies indicated that Porphyromonas gingivalis (Pg) induced insulin secretion in MIN6 β cells and this induction was in part SerpinE1 (plasminogen activator inhibitor 1, PAI1) dependent. However, the mechanism(s) by which periodontitis induces prediabetes is not known. Since α and β cells in pancreatic islets are the major modulators of glucose levels, we investigated whether experimental periodontitis by oral application of a periodontal pathogen caused molecular and/or cellular alterations in pancreatic islets and whether SerpinE1 was involved in this process.