Maternal fructose drives placental uric acid production leading to adverse fetal outcomes

• DOI: 10.1038/srep25091
• Publication Date: 2016-04-29T09:59:51Z
• Authors: Zeenat A. Asghar; Alysha Thompson; Maggie Chi; Andrew Cusumano; Suzanne Scheaffer; Noor Al-Hammadi; Jessica L. Saben; Kelle H. Moley
• Keywords: Allopurinol

Abstract Maternal metabolic diseases increase offspring risk for low birth weight and cardiometabolic in adulthood. Excess fructose consumption may confer risks both women their offspring. However, the direct consequences of intake per se are unknown. We assessed impact a maternal high-fructose diet on fetal-placental unit mice absence syndrome determined association between serum placental uric acid levels humans. In mice, led to inefficiency, fetal growth restriction, elevated glucose triglyceride levels. placenta, induced de novo synthesis by activating activities enzymes AMP deaminase xanthine oxidase. Moreover, placentas had increased lipids altered expression genes that control oxidative stress. Treatment mothers with oxidase inhibitor allopurinol reduced levels, prevented inefficiency improved weights triglycerides. Finally, 18 delivering at term, significantly correlated These findings suggest excess impairs function via oxidase/uric acid-dependent mechanism similar effects occur