Abstract
Current evidence indicates that chemical pollutants may interfere with the homeostatic control of nutrient metabolism, thereby contributing to the increased prevalence of metabolic disorders. Bisphenol-A (BPA) is a lipophilic compound contained in plastic which is considered a candidate for impairing energy and glucose metabolism. We have investigated the impact of low doses of BPA on adipocyte metabolic functions. Human adipocytes derived from subcutaneous adipose tissue and differentiated 3T3-L1 cells were incubated with BPA, in order to evaluate the effect on glucose utilization, insulin sensitivity and cytokine secretion. Treatment with 1nM BPA significantly inhibited insulin-stimulated glucose utilization, without grossly interfering with adipocyte differentiation. Accordingly, mRNA levels of the adipogenic markers PPARγ and GLUT4 were unchanged upon BPA exposure. BPA treatment also impaired insulin-activated receptor phosphorylation and signaling. Moreover, adipocyte incubation with BPA was accompanied by increased release of IL-6 and IFN-γ, as assessed by multiplex ELISA assays, and by activation of JNK, STAT3 and NFkB pathways. Treatment of the cells with the JNK inhibitor SP600125 almost fully reverted BPA effect on insulin signaling and glucose utilization. In conclusion, low doses of BPA interfere with inflammatory/insulin signaling pathways, leading to impairment of adipose cell function.
Highlights
Overweight, obesity and insulin resistance epidemics are significant human health problems in adults, and in children and adolescents [1,2]
Insulin stimulatory effect was still detectable after 8h incubation with 1 nM BPA, while after 24h of incubation with BPA, insulin effect on glucose utilization was reduced by 55% (Fig 1a).Within the same time frame, 100 nM BPA decreased insulin stimulatory action by .70%
It is possible that pollutants may participate in deranging the function of adipose tissue, contributing to the inflammatory condition and to insulin resistance
Summary
Overweight, obesity and insulin resistance epidemics are significant human health problems in adults, and in children and adolescents [1,2]. They are associated with increased risk of diseases related to metabolic dysfunctions, including metabolic syndrome (MS), type 2 diabetes mellitus (T2D), coronary heart disease (CHD), and some forms of cancer [3,4,5,6]. Chronic inflammation often accompanies obesity and related disorders, suggesting that inflammatory factors might be a crucial culprit connecting adipose tissue dysfunction with insulin resistance and diabetes as well as with cardiovascular disease and cancer [5,6,7,8,9]. An even larger impact could be exerted by those which are resistant to biological and chemical degradation, termed Persistent Organic Pollutants(POPs), most of them classified as endocrine disruptors [15,16,17,18,19,20]
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