Figure 4.

Hypothetical model of how the early phenotype induced by bisphenol-A (BPA) may contribute to metabolic alterations later in life. Bisphenol-A treatment of pregnant mice exacerbates insulin resistance in mothers (81) and can cross the placental barrier and produce effects in fetuses. As a consequence of these BPA actions, there is a modification of the expression of genes involved in cell division and function that should contribute to early hyperinsulinemia, increased β-cell mass and decreased glucose-stimulated insulin secretion (GSIS) (89). This early hyperinsulinemia should contribute to weight gain later in life, as well as glucose intolerance, dyslipidemima, insulin resistance, and fatty liver that have been demonstrated in adult male mice in many different studies. Created with BioRender.com.