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Published on: June 3, 2016
Bisphenol A is associated with insulin resistance and modulates adiponectin and resistin gene expression in obese
Ciro Menale1,2,3, Anna Grandone4, Carla Nicolucci1,2,5
1Department of Experimental Medicine, Second University of Naples, Naples, Italy.
Insights
Bisphenol A (BPA) exposure in obese children is linked to higher insulin resistance and altered adiponectin levels. BPA affects resistin and adiponectin gene expression in fat cells, suggesting a role in childhood obesity.
Area of Science:
- Endocrinology
- Environmental Health
- Pediatrics
Background:
- Bisphenol A (BPA) exposure is linked to increased diabetes and obesity in adults.
- Investigating BPA's role in pediatric metabolic dysfunction is crucial.
Purpose of the Study:
- To evaluate the association between urinary BPA levels and insulin resistance in obese children.
- To assess BPA's impact on adiponectin and resistin production and serum concentrations.
- To examine BPA's effect on adiponectin and resistin gene expression in human adipocytes.
Main Methods:
- Collected clinical and biochemical data from 141 obese children.
- Measured serum resistin and adiponectin, and urinary BPA levels.
- Used quantitative real-time RT-PCR (qPCR) to analyze gene expression in adipocytes.
Main Results:
- Found a direct association between BPA and insulin resistance (homeostasis model assessment).
- Observed a strong inverse association between BPA and adiponectin levels.
- BPA exposure in adipocytes induced resistin expression and suppressed adiponectin expression.
Conclusions:
- BPA may contribute to insulin resistance in childhood obesity.
- Urinary BPA levels correlate with insulin resistance independently of BMI.
- BPA's influence on resistin and adiponectin production in adipose tissue may explain these associations.
Background:
Bisphenol A (BPA) exposure has been associated with increased incidence of diabetes and obesity in adults.
Objectives:
To evaluate whether an association between BPA urinary levels and insulin resistance as well as adiponectin and resistin production and serum concentrations may occur in obese children.
Methods:
Clinical and biochemical features of 141 obese children were collected. Serum resistin and adiponectin were evaluated. Insulin resistance and urinary BPA levels were assessed. Moreover, the effect of BPA on adiponectin and resistin gene expression in adipocytes from eight normal weight prepubertal children was investigated by quantitative real-time RT-PCR (qPCR).
Results:
Direct association between BPA and homeostasis model assessment (r = 0.23; p: 0.0069) and a strong inverse association between BPA and adiponectin have been found (r = -0.48; p < 0.0001). In adipocytes, resistin expression was detected only after BPA treatment, while adiponectin expression resulted down-regulated after BPA exposure (p < 0.05 at both 10 and 100 nM BPA concentrations).
Conclusions:
We suggest the involvement of BPA in the development of insulin resistance in childhood obesity highlighting that urinary BPA levels are directly associated with insulin resistance regardless of BMI. This association may be explained, at least partly, by the findings that BPA affects resistin and adiponectin production in adipose tissue cultures.
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