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Updated: Jan 6, 2026

Moderate Prenatal Alcohol Exposure and Quantification of Social Behavior in Adult Rats
Published on: December 14, 2014
Prenatal fructose exposure independently impacts placental phenotype and female offspring kidney function and liver
A Augusto Coppi1, Clint Gray2,3, Aliny A B Lobo Ladd4
1Faculty and Health and Life Sciences, University of Bristol, Bristol, UK.
Abstract:
Archaeological and anthropological evidence suggests that human ancestors' diets were rich in fiber, potassium, and complex carbohydrates, while low in sodium, refined sugars, and energy density. Over time, agroindustrialization led to diets poorer in fiber and micronutrients but higher in sodium, simple sugars, and calorie-dense foods. This shift contributed to the rise of noncommunicable diseases (NCDs) such as obesity, type 2 diabetes, and cardiovascular diseases, which now account for 70% of global premature deaths. Maternal nutrition affects fetal development and long-term health. High sucrose or fructose intake during pregnancy can alter placental function, impacting fetal growth and metabolism. Placentae from male and female fetuses may respond differently to maternal diet. However, the effects of excessive maternal fructose intake on the placenta and offspring remain underexplored. In this study, rat dams consuming fructose-sweetened beverages ate less food but drank more, significantly impacting placental volume and vascular structure. Long-term effects on offspring were sex-specific: females showed greater water retention and liver fat accumulation. High maternal fructose intake altered placental anatomy and had sex-specific effects on kidney and liver function in adult offspring, even without further fructose exposure. These findings highlight the importance of maternal diet in preventing future metabolic diseases.
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