Maternal apical periodontitis is associated with insulin resistance in adult offspring

Abstract

Aim To investigate the plasma concentrations of glucose, insulin and tumour necrosis factor‐α (TNF‐α) of rats with maternal apical periodontitis (AP) and to explore the effect of maternal inflammation on the initial steps of insulin signalling and the inflammatory pathway in the gastrocnemius muscle (GM) and periepididymal white adipose tissue (pWAT) of adult offspring. Methodology Fifteen female Wistar rats were distributed into a control group (CN), a group with 1 tooth with AP (1AP) and a group with 4 teeth with 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 homoeostasis 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 and pWAT were measured by Western blot. Analysis of variance was performed, followed by the Tukey's post hoc test. P values <0.05 were considered to be statistically significant. Results Maternal AP promoted insulin resistance, impaired the initial steps of insulin signalling, significantly increased plasma concentrations of insulin (P < 0.001) and TNF‐α (P < 0.05), and enhanced IKKα/β phosphorylation in the GM and pWAT (P < 0.05) of adult offspring. However, maternal AP did not affect fasting glycaemia and JNK phosphorylation in the GM and pWAT of adult offspring. Conclusions Maternal AP was associated with insulin resistance in adult offspring through alterations in insulin signalling and inflammation pathways. The study provides information on the impact of maternal AP on the development of metabolic alterations such as insulin resistance in adult offspring and reinforces the importance of preventing maternal AP in order to maintain the general health of offspring.

Effects of melatonin on insulin signaling and inflammatory pathways of rats with apical periodontitis

“…Another study reported that in adult rats, the offspring of rats with AP had insulin resistance, increased plasma concentration of TNF‐α, changes in the inflammatory pathway (increased IKKα/β phosphorylation status) and insulin signalling (decreased pp185 tyrosine phosphorylation status and increased IRS‐1 serine phosphorylation status) in muscle tissue and WAT (Tsosura et al . 2019).…”

“…Similarly, there were no differences in this parameter in muscle tissue of adult rats, offspring of rats with AP (Tsosura et al . 2019) or PD (Mattera et al . 2019).…”

Effect of maternal apical periodontitis on the final step of insulin signalling and inflammatory pathway in the adult male offspring of rats

“…In a previous study, there was an increase in the TNF‐α plasma concentration in the 1AP‐o and 4AP‐o groups compared with the CN‐o group (Tsosura et al, 2019). However, in the present study, there was no difference in TNF‐α gene expression and its protein content in the GM amongst the groups, indicating that the GM is not a source of this inflammatory cytokine, and other tissues, such as the adipose tissue, may contribute to the increase in the TNF‐α plasma concentration.…”

“…Tsosura et al (2019) reported that maternal apical periodontitis (AP) was associated with IR, increased TNF‐α plasma concentration, impairment in the initial step of insulin signalling and activation of the inflammatory pathway (IKKα/β) in the gastrocnemius muscle (GM) of adult offspring of rats. However, the mechanisms involved in this IR are not fully understood.…”

“…Peroxisome proliferator-activated receptor-gamma coactivator 1 (PGC-1) mediates the increase in GLUT4 gene expression by binding to and coactivating the myocyte enhancer factor 2C (MEF2C). [Colour figure can be viewed at wileyonlinelibrary.com] Tsosura et al (2019) reported that maternal apical periodontitis (AP) was associated with IR, increased TNF-α plasma concentration, impairment in the initial step of insulin signalling and activation of the inflammatory pathway (IKKα/β) in the gastrocnemius muscle (GM) of adult offspring of rats. However, the mechanisms involved in this IR are not fully understood.…”