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 signaling 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 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 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 signaling, 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 glycemia 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 signaling 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.
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