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Introduction Over the past decade, the incidence of diabetes has increased dramatically. The WHO estimates mortality due to diabetes to increase by 50% in the next 10 y, making it a major cause of death by 2030 and placing a substantial economic burden on the health care system globally (Mathers and Loncar 2006; American Diabetes Association 2013). Therefore, understanding the underlying factors of this global epidemic is critical.
Accumulating evidence has suggested that a suboptimal early life environment produces multigenerational developmental defects. A proposed mechanism is stable inheritance of DNA methylation. Here we show that maternal bisphenol A (BPA) exposure in C57BL/6 mice produces multigenerational metabolic phenotypes in their offspring.
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