Serpine1 Mediates XXXX Induced Insulin Secretion in the Pancreatic Beta Cell Line MIN6.

@entity32 @entity558 @entity6 @entity73236 @entity604 @entity3190 @entity2521 @entity1602 @entity2523
UNASSIGNED: Periodontitis is an @entity32 resulting in destruction of @entity604 caused by an exuberant host immunological response to periodontal pathogens. Results from a number of epidemiological studies indicate a close association between @entity6 and @entity2521 . Results from cross-sectional studies indicate that subjects with @entity2521 have a higher odds ratio of developing insulin resistance (IR). However, the mechanisms by which @entity2521 influences the development of @entity6 are not known. Results from our previous studies using an animal model of @entity2521 suggest that @entity2521 accelerates the onset of @entity3190 and IR. In addition, @entity558 from a periodontal pathogen, @entity2523 (Pg), stimulates Serpine1 expression in the pancreatic beta cell line MIN6. Based on these observations, we hypothesized that a periodontal pathogen induces @entity3190 and @entity73236 may be involved in this process. To test this hypothesis, we co-incubated Pg with the pancreatic beta cell line MIN6 and measured the effect on insulin secretion by MIN6 cells. We further determined the involvement of Serpine1 in insulin secretion by downregulating Serpine1 expression. Our results indicated that Pg stimulated insulin secretion by approximately 3.0 fold under normoglycemic conditions. In a @entity1602 state, Pg increased insulin secretion by 1.5 fold. Pg significantly upregulated expression of the Serpine1 gene and this was associated with increased secretion of insulin by MIN6 cells. However, cells with downregulated Serpine1 expression were resistant to Pg stimulated insulin secretion under normoglycemic conditions. We conclude that the periodontal pathogen, Pg, induced insulin secretion by MIN6 cells and this induction was, in part, Serpine1 dependent. Thus, Serpine1 may play a pivotal role in insulin secretion during the accelerated development of @entity3190 and the resulting IR in the setting of @entity2521 .
