Prenatal sensitization of a postnatal trigger for metabolic disease
Susan K. Murphy
Susan K. Murphy
Published June 24, 2013
Citation Information: J Clin Invest. 2013;123(7):2786-2788. https://doi.org/10.1172/JCI69399.
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Commentary

Prenatal sensitization of a postnatal trigger for metabolic disease

Abstract

Intrahepatic cholestasis of pregnancy (ICP), marked by elevated maternal serum bile acid levels, occurs in late pregnancy and is often associated with poor perinatal outcomes. In this issue of the JCI, Papacleovoulou et al. analyze the long-term consequences of ICP and find that teens born to mothers with ICP exhibit enhanced characteristics of metabolic syndrome relative to controls. The authors also used a new ICP mouse model to support and extend these findings, demonstrating that in utero exposure to bile acids induces persistent epigenetic alterations and abnormal placental lipogenesis, setting the stage for later metabolic dysfunction.

Authors

Susan K. Murphy

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Figure 1

Exposure to bile acids in utero leads to metabolic profile reprogramming in the developing child, likely through epigenetic alterations.

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Exposure to bile acids in utero leads to metabolic profile reprogramming...
This reprogramming establishes a diet-sensitive trigger that responds to poor dietary choice by increasing the likelihood of developing metabolic syndrome. The manifestation of this syndrome may be constrained by consumption of a healthy diet.