Bisphenol a: A narrative review of prenatal exposure effects on adipogenesis and childhood obesity via peroxisome proliferator-activated receptor gamma

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

There is significant evidence of globally ubiquitous prenatal exposures to bisphenol A (BPA). Childhood obesity as an epidemic has been a global concern for over a decade. Experimental models and epidemiological evidence suggest that BPA may act as an obesogen during adipogenesis. Results from stem cell models and birth cohort studies support the developmental origins of health and disease theory. While literature reviews have presented a variety of potential mechanisms of BPA action during adipogenesis, there remains no consensus. This review is the first to explore the proliferator-activated receptor gamma (PPARγ) mechanism in detail. This review will also examine the obesogenic effect of prenatal exposure to BPA during critical windows of vulnerability. Although vast experimental literature exists, there is limited epidemiological evidence to support the hypothesis for the obesogenic effect of BPA. The primary goal of this review is to provide researchers with a roadmap of existing research and suggestions for future directions for analyzing the relationship between prenatal BPA exposures and childhood obesity.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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