Abstract
Results from epidemiological and prospective studies indicate a close association between periodontitis and diabetes. However the mechanisms by which periodontal pathogens influence the development of prediabetes/diabetes are not clear. We previously reported that oral administration of a periodontal pathogen, Porphyromonas gingivalis (Pg) to WT mice results in insulin resistance, hyperinsulinemia, and glucose intolerance and that Pg translocates to the pancreas. In the current study, we determined the specific localization of Pg in relation to mouse and human pancreatic α- and β-cells using 3-D confocal and immunofluorescence microscopy and orthogonal analyses. Pg/gingipain is intra- or peri-nuclearly localized primarily in β-cells in experimental mice and also in human post-mortem pancreatic samples. We also identified bihormonal cells in experimental mice as well as human pancreatic samples. A low percentage of bihormonal cells has intracellular Pg in both humans and experimental mice. Our data show that the number of Pg translocated to the pancreas correlates with the number of bihormonal cells in both mice and humans. Our findings suggest that Pg/gingipain translocates to pancreas, particularly β-cells in both humans and mice, and this is strongly associated with emergence of bihormonal cells.
Highlights
Results from epidemiological and prospective studies indicate a close association between periodontitis and diabetes
Periodontitis is a disease characterized by destruction of gingiva and tooth-supporting bone by a host immunological response triggered by periodontal pathogens
We have recently determined that mice orally administered Porphyromonas gingivalis (Pg) develop insulin resistance and hyperinsulinemia while maintaining normal glucose levels indicating a prediabetic condition[11] and that Pg translocates to the pancreas[12]
Summary
Results from epidemiological and prospective studies indicate a close association between periodontitis and diabetes. We have recently shown that Pg orally administered to mice is translocated to the brain and is localized peri- and intra-nuclearly in neurons, astrocytes and microglial cells in the hippocampus and this is associated with the development of senile plaques[5] This suggests that Pg/gingipain is able to invade cells in distant organs and may result in a pathological conditions. We have recently determined that mice orally administered Pg develop insulin resistance and hyperinsulinemia while maintaining normal glucose levels indicating a prediabetic condition[11] and that Pg translocates to the pancreas[12] These results suggest that Pg may influence β-cell function. A recent study using human pancreatic samples obtained following pancreatoduodenectomy reported the higher percentage of bihormonal cells in an insulin resistant group compared with an insulin sensitive group, suggesting a possible adaptive response to insulin resistance[23]
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