Endocrine

, Volume 44, Issue 1, pp 79–86

Fructose intake during pregnancy up-regulates the expression of maternal and fetal hepatic sterol regulatory element-binding protein-1c in rats

Authors

    • Department of NutritionFaculty of Health Sciences, Aomori University of Health and Welfare
  • Maya Kumazawa
    • Department of NutritionFaculty of Health Sciences, Aomori University of Health and Welfare
  • Shin Sato
    • Department of NutritionFaculty of Health Sciences, Aomori University of Health and Welfare
Original Article

DOI: 10.1007/s12020-012-9815-8

Cite this article as:
Mukai, Y., Kumazawa, M. & Sato, S. Endocrine (2013) 44: 79. doi:10.1007/s12020-012-9815-8

Abstract

Excess fructose consumption is associated with the development of type 2 diabetes and obesity. However, the impact of fructose intake on maternal and fetal lipid metabolism during pregnancy is not known. The aim of this study was to examine whether maternal fructose intake during pregnancy would affect fetal and maternal hepatic lipid metabolism. Pregnant Wistar rats were randomly divided into untreated control and fructose-treated groups; the fructose-treated group received fructose via drinking water throughout pregnancy. On gestational day 20, glucose and insulin concentration in the maternal plasma were measured. The mRNA expression of sterol regulatory element-binding protein (SREBP)-1c and its target genes in the liver of dams and fetuses were analyzed by real-time PCR. Significantly higher maternal plasma glucose levels, indicating hyperglycemia, was observed in the fructose-treated group than in the control group. Furthermore, the fructose-treated group showed significantly higher expression levels of both maternal and fetal SREBP-1c mRNA and protein and significantly elevated expression of fatty acid synthase; the group also showed reduced acyl-CoA oxidase levels in the maternal liver. Thus, our results suggest that maternal fructose intake during pregnancy causes maternal hyperglycemia and up-regulates hepatic SREBP-1c expression in both fetuses and dams. This may lead to defects in carbohydrate and lipid metabolism in the adult offspring.

Keywords

FructoseRatSREBP-1cFetusLiverLipid metabolism

Copyright information

© Springer Science+Business Media New York 2012