Maternal fructose drives placental uric acid production leading to adverse fetal outcomes
Autor: | Suzanne M. Scheaffer, Kelle H. Moley, Zeenat Asghar, Noor Al-Hammadi, Alysha Thompson, Maggie M.-Y. Chi, Jessica Saben, Andrew Cusumano |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Xanthine Oxidase medicine.drug_class Allopurinol Placenta 030209 endocrinology & metabolism Placental insufficiency Fructose Biology Article AMP Deaminase 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Pregnancy Internal medicine medicine Animals Xanthine oxidase Xanthine oxidase inhibitor Triglycerides 2. Zero hunger Multidisciplinary Fetal Growth Retardation medicine.disease Placental Insufficiency 3. Good health Uric Acid Disease Models Animal Oxidative Stress 030104 developmental biology Endocrinology medicine.anatomical_structure chemistry Uric acid Female Metabolic syndrome medicine.drug |
Zdroj: | Scientific Reports |
ISSN: | 2045-2322 |
Popis: | Maternal metabolic diseases increase offspring risk for low birth weight and cardiometabolic diseases in adulthood. Excess fructose consumption may confer metabolic risks for both women and their offspring. However, the direct consequences of fructose intake per se are unknown. We assessed the impact of a maternal high-fructose diet on the fetal-placental unit in mice in the absence of metabolic syndrome and determined the association between maternal serum fructose and placental uric acid levels in humans. In mice, maternal fructose consumption led to placental inefficiency, fetal growth restriction, elevated fetal serum glucose and triglyceride levels. In the placenta, fructose induced de novo uric acid synthesis by activating the activities of the enzymes AMP deaminase and xanthine oxidase. Moreover, the placentas had increased lipids and altered expression of genes that control oxidative stress. Treatment of mothers with the xanthine oxidase inhibitor allopurinol reduced placental uric acid levels, prevented placental inefficiency and improved fetal weights and serum triglycerides. Finally, in 18 women delivering at term, maternal serum fructose levels significantly correlated with placental uric acid levels. These findings suggest that in mice, excess maternal fructose consumption impairs placental function via a xanthine oxidase/uric acid-dependent mechanism and similar effects may occur in humans. |
Databáze: | OpenAIRE |
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