High fructose consumption in pregnancy alters the perinatal environment without increasing metabolic disease in the offspring
Christopher Lineker A , Paul M. Kerr B G , Patricia Nguyen B , Ian Bloor F , Stuart Astbury A F , Nikhil Patel A F , Helen Budge F , Denise G. Hemmings C D E , Frances Plane B D E , Michael E. Symonds F and Rhonda C. Bell A E H
+ Author Affiliations
- Author Affiliations
A Division of Human Nutrition, Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, Alberta T6G 2E1, Canada.
B Department of Pharmacology, University of Alberta, Edmonton, Alberta T6G 2E1, Canada.
C Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Alberta T6G 2E1, Canada.
D Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta T6G 2E1, Canada.
E Women and Children’s Health Research Institute, University of Alberta, Edmonton, Alberta T6G 2E1, Canada.
F Early Life Research Group, Academic Division of Child Health, Obstetrics and Gynaecology, School of Medicine, Queen’s Medical Centre, University Hospital, The University of Nottingham, Nottingham NG7 2UH, UK.
G Present address: Faculty of Health and Community Studies, MacEwan University, Robbins Health Learning Centre, Edmonton, Alberta T5J 4S2, Canada.
H Corresponding author. Email: rhonda.bell@ualberta.ca
Reproduction, Fertility and Development 28(12) 2007-2015 https://doi.org/10.1071/RD15119
Submitted: 26 March 2015 Accepted: 4 June 2015 Published: 6 July 2015
Abstract
Maternal carbohydrate intake is one important determinant of fetal body composition, but whether increased exposure to individual sugars has long-term adverse effects on the offspring is not well established. Therefore, we examined the effect of fructose feeding on the mother, placenta, fetus and her offspring up to 6 months of life when they had been weaned onto a standard rodent diet and not exposed to additional fructose. Dams fed fructose were fatter, had raised plasma insulin and triglycerides from mid-gestation and higher glucose near term. Maternal resistance arteries showed changes in function that could negatively affect regulation of blood pressure and tissue perfusion in the mother and development of the fetus. Fructose feeding had no effect on placental weight or fetal metabolic profiles, but placental gene expression for the glucose transporter GLUT1 was reduced, whereas the abundance of sodium-dependent neutral amino acid transporter-2 was raised. Offspring born to fructose-fed and control dams were similar at birth and had similar post-weaning growth rates, and neither fat mass nor metabolic profiles were affected. In conclusion, raised fructose consumption during reproduction results in pronounced maternal metabolic and vascular effects, but no major detrimental metabolic effects were observed in offspring up to 6 months of age.
Additional keywords: developmental origins, fetal programming, metabolism, vascular function.
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