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PLoS One. 2013 Dec 9;8(12):e82099. doi: 10.1371/journal.pone.0082099. eCollection 2013.

Bisphenol-A impairs insulin action and up-regulates inflammatory pathways in human subcutaneous adipocytes and 3T3-L1 cells.

Author information

1
Istituto di Endocrinologia ed Oncologia Sperimentale (IEOS-CNR), Naples, Italy.
2
Dipartimento di Scienze Mediche Traslazionali, Università degli Studi di Napoli "Federico II", Naples, Italy.
3
Dipartimento di Scienze Mediche Traslazionali, Università degli Studi di Napoli "Federico II", Naples, Italy ; Dipartimento di Scienze Farmaceutiche, Università degli Studi di Salerno, Salerno, Italy.
4
Istituto di Endocrinologia ed Oncologia Sperimentale (IEOS-CNR), Naples, Italy ; Dipartimento di Scienze Mediche Traslazionali, Università degli Studi di Napoli "Federico II", Naples, Italy.

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 1 nM 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.

PMID:
24349194
PMCID:
PMC3857211
DOI:
10.1371/journal.pone.0082099
[Indexed for MEDLINE]
Free PMC Article

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