AI Article Synopsis

  • Recent studies highlight a strong link between periodontitis and diabetes, though the exact mechanisms remain unclear.
  • Administration of the periodontal pathogen Porphyromonas gingivalis (Pg) in mice leads to conditions like insulin resistance and glucose intolerance, with Pg found in the pancreas.
  • Research using advanced microscopy techniques reveals Pg mainly localizes in pancreatic β-cells, and its presence correlates with the emergence of bihormonal cells in both mice and human samples.

Article 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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305306PMC
http://dx.doi.org/10.1038/s41598-020-65828-xDOI Listing

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