1774-P: Maternal Apical Periodontitis Promotes Insulin Resistance in Adult Offspring

Abstract

Background: Adverse stimuli applied during early fetal development can increase the risk of diseases in adulthood. Aim: This study investigated the plasma concentrations of glucose, insulin, and tumor necrosis factor-α (TNF-α) of rats with maternal apical periodontitis (AP). We also explored the effect of maternal inflammation on the initial steps of insulin signaling and the inflammatory pathway in the gastrocnemius muscle (GM) of adult offspring. Methodology: Fifteen female Wistar rats were distributed into control group (CN), group with 1 AP (1AP) and group with 4 AP (4AP). Thirty days following induction of AP, female rats from all groups were mated with healthy male rats. When male offspring reached 75 days of age, plasma concentrations of glucose, insulin, and TNF-α were quantified. Insulin resistance was evaluated by the homeostasis model assessment of insulin resistance (HOMA-IR) index. Phosphorylation status of pp185 tyrosine, insulin receptor substrate 1 (IRS-1) serine, IκB kinase α/β (IKKα/β), and c-Jun N-terminal kinase (JNK) in the GM were measured by western blot. Results: Maternal AP promotes insulin resistance, impairs the initial steps of insulin signaling, increases plasma concentrations of insulin and TNF-α, and enhances IKKα/β phosphorylation in the GM of adult offspring. However, maternal AP does not seem to affect fasting glycemia and JNK phosphorylation in the GM of adult offspring. Conclusions: Maternal AP promotes important alterations in insulin signaling and inflammation pathways, and leads to insulin resistance in adult offspring. Disclosure T.V. Tsosura: None. F.Y. Chiba: None. M.S. Mattera: None. R.F. Pereira: None. C.A. Garbin: None. L.T. Cintra: None. D.H. Sumida: None. Funding São Paulo Research Foundation (2017-01128-1)