BackgroundMost studies have investigated the association between parental socioeconomic factors and dental caries in children based on educational and income levels; studies focusing on parental occupation, however, have been relatively limited. This cross-sectional study examined the associations between parental occupations and levels of education and household income and the prevalence of dental caries in Japanese children aged 3 years.MethodsStudy subjects were 6315 children. Oral examination results were obtained from the parents or guardians, who transcribed the information recorded by medical staff at a public health center from their maternal and child health handbooks to our self-administered questionnaire. Children were classified as having dental caries if one or more primary teeth had decayed or had been filled. Adjustment was made for sex, age, region of residence, breastfeeding duration, between-meal snack frequency, toothbrushing frequency, use of fluoride, regular dental check-ups, maternal smoking during pregnancy, and living with at least one household smoker.ResultsThe prevalence of dental caries was 14.7%. Compared with having an unemployed father, having a father employed in professional and engineering, clerical, sales, security, or manufacturing process was significantly associated with a lower prevalence of dental caries. Compared with having an unemployed mother, having a mother employed in professional and engineering or service was significantly inversely associated with the prevalence of dental caries. Significant inverse associations were observed between parental levels of education and household income and the prevalence of dental caries.ConclusionsThe findings of our study suggest that parental occupation affects the prevalence of dental caries in children. We confirm that higher levels of parental education and household income decreased the prevalence of dental caries.
Visceral adipose tissue (VAT) inflammation has been linked to the pathogenesis of insulin resistance and metabolic syndrome. VAT has recently been established as a new component of the immune system and is involved in the production of various adipokines and cytokines. These molecules contribute to inducing and accelerating systemic insulin resistance. In this report, we investigated the role of B cell‐activating factor (BAFF) in the induction of insulin resistance. We investigated BAFF levels in the sera and VAT of obese mice. In obese mice, the BAFF levels were preferentially increased in VAT and sera compared to these levels in normal control mice. Next, we treated mice with BAFF to analyze its influence on insulin sensitivity. BAFF impaired insulin sensitivity in normal mice. Finally, we investigated the mechanisms underlying insulin resistance induced by BAFF in adipocytes. BAFF also induced alterations in the expression levels of genes related to insulin resistance in adipocytes. In addition, BAFF directly affected the glucose uptake and phosphorylation of insulin receptor substrate‐1 in adipocytes. We propose that autocrine or paracrine BAFF and BAFF‐receptor (BAFF‐R) interaction in VAT leads to impaired insulin sensitivity via inhibition of insulin signaling pathways and alterations in adipokine production.
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