Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile
Article first published online: 12 JUL 2013
© 2013 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd
Special Issue: Metabolic Programming
Volume 210, Issue 1, pages 142–153, January 2014
How to Cite
Kjaergaard, M., Nilsson, C., Rosendal, A., Nielsen, M. O. and Raun, K. (2014), Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile. Acta Physiologica, 210: 142–153. doi: 10.1111/apha.12138
- Issue published online: 13 DEC 2013
- Article first published online: 12 JUL 2013
- Accepted manuscript online: 19 JUN 2013 07:10AM EST
- Manuscript Accepted: 13 JUN 2013
- Manuscript Revised: 28 MAY 2013
- Manuscript Revised: 1 MAR 2013
- Manuscript Received: 4 FEB 2013
- Danish Council for Strategic Research. Grant Number: 09 067124
- The Research School of Animal Nutrition and Physiology, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark, and Novo Nordisk Training and Research Program (TRAP), NOVO Nordisk A/S, Gentofte, Denmark, and the Danish Society for Science, Technology and Innovation
- hepatic steatosis;
- lipid homeostasis;
- litter size reduction;
- maternal high-fat/high-sucrose diet
According to the World Diabetes Foundation, there is an urgent need to investigate the impact of maternal health and nutrition during pregnancy to understand the background for the accelerating incidence of obesity and type 2 diabetes. In this study, we specifically concentrated on the role of overfeeding during different developmental periods.
Sprague–Dawley rats were offered chow or high-fat/high-sucrose diet (chow plus chocolate and soft drink) during gestation and lactation. At birth, offspring were randomly cross-fostered within each dietary group into small and normal litter sizes until weaning, giving four dietary groups.
At postnatal day 1, offspring from high-fat/high-sucrose-fed dams were heavier and had increased hepatic triglycerides (TG), hepatic glycogen, blood glucose and plasma insulin compared with offspring from chow-fed dams. Hepatic genes involved in lipid oxidation, VLDL transport and insulin receptor were down-regulated, whereas FGF21 expression was up-regulated. Independent of postnatal litter size, offspring from high-fat/high-sucrose-fed dams aged 21 days had still increased hepatic TG and up-regulated FGF21 expression, while plasma insulin started to decrease. Litter size reduction in offspring from high-fat/high-sucrose-fed dams further increased body weight and adiposity, and up-regulated genes involved in hepatic mitochondrial lipid oxidation and VLDL transport compared with all other groups. Litter size reduction did not have any impact on body weight gain and adiposity in offspring born to chow-fed dams.
Our results suggest that supplementation of chocolate and soft drink during gestation and lactation contributes to early onset of hepatic steatosis associated with changes in hepatic gene expression and lipid handling.