Bisphenol-A (BPA) is one of the most widespread endocrine disrupting chemicals 
(EDC) used as the base compound in the manufacture of polycarbonate plastics. 
Although evidence points to consider exposure to BPA as a risk factor for 
insulin resistance, its actions on whole body metabolism and on 
insulin-sensitive tissues are still unclear. The aim of the present work was to 
study the effects of low doses of BPA in insulin-sensitive peripheral tissues 
and whole body metabolism in adult mice. Adult mice were treated with 
subcutaneous injection of 100 µg/kg BPA or vehicle for 8 days. Whole body energy 
homeostasis was assessed with in vivo indirect calorimetry. Insulin signaling 
assays were conducted by western blot analysis. Mice treated with BPA were 
insulin resistant and had increased glucose-stimulated insulin release. 
BPA-treated mice had decreased food intake, lower body temperature and locomotor 
activity compared to control. In skeletal muscle, insulin-stimulated tyrosine 
phosphorylation of the insulin receptor β subunit was impaired in BPA-treated 
mice. This impairment was associated with a reduced insulin-stimulated Akt 
phosphorylation in the Thr(308) residue. Both skeletal muscle and liver 
displayed an upregulation of IRS-1 protein by BPA. The mitogen-activated protein 
kinase (MAPK) signaling pathway was also impaired in the skeletal muscle from 
BPA-treated mice. In the liver, BPA effects were of lesser intensity with 
decreased insulin-stimulated tyrosine phosphorylation of the insulin receptor β 
subunit.In conclusion, short-term treatment with low doses of BPA slows down 
whole body energy metabolism and disrupts insulin signaling in peripheral 
tissues. Thus, our findings support the notion that BPA can be considered a risk 
factor for the development of type 2 diabetes.