Proceedings of The Physiological Society
University College Dublin (2009) Proc Physiol Soc 15, PC22
The effect of increased fructose and/or salt intake on maternal liver and plasma lipids in rats
C. Gray1, M. E. Symonds2, S. M. Gardiner3, D. S. Gardner1
1. School of Veterinary Medicine & Science, Nottingham University, Nottingham, United Kingdom. 2. School of Clinical Sciences, Nottingham University, Nottingham, United Kingdom. 3. School of Biomedical Sciences, Nottingham University, Nottingham, United Kingdom.
The prevalence of non-alcoholic fatty liver disease (NAFLD) in the developed world has markedly increased. NAFLD is a multi-factorial disease but a specific causal link has been made to increased fructose consumption(1). A major concern for women living in a contemporary western society is excess nutrient availability, especially salt and simple sugars (such as fructose). The present study has therefore examined the effect of increased maternal salt and fructose intake on maternal metabolism and growth. 32 virgin Sprague Dawley rats (~180g) were randomly divided into 4 dietary groups; 1) control diet (CD, n=8) fed purified chow and tap water, 2) salt diet (SD, n=8) fed purified chow containing 4% NaCl and tap water, 3) fructose diet (FD, n=8) fed purified chow and 10% fructose in tap water and 4) fructose & salt diet (FSD, n=8), fed 4% NaCl purified chow with 10% fructose in tap water. Animals were fed ad libitum for 28 days prior to conception, mated and maintained on experimental diets until day 20 of gestation, whereupon they were euthanized. Blood samples were taken 14 days prior to conception and at day 20 of gestation for analysis of protein, fat and carbohydrate metabolism using an auto analyser (RX-IMOLA, Randox). Prior to feeding the experimental diets, there was no significant difference between the body weights of dams (220±10g). During pregnancy all animals gained a similar amount of weight (115±6g). Prior to pregnancy, fructose intake increased triglyceride (P<0.001) in FD (1.064±0.08mmol/l) and FSD (0.911±0.11mmol/l) when compared to CD (0.72±0.08mmol/l ). NEFA was also increased (P<0.001) in FD (0.67±0.04 mmol/l) when compared to CD (0.55±0.04mmol/l). Maternal liver wet weight was specifically increased 20-25% (P<0.001) by the consumption of fructose, FD (15.22±0.32g), FSD (14.64±0.32g) vs. CD (12.17±0.37g). In addition, a significant redistribution of adipose tissue in the dams consuming excess fructose was observed; relative to CD, the gonadal depot in FD was reduced (FD, 4.91±0.51g vs. CD, 7.15±0.59) but perirenal depot increased (FD, 2.96±0.11g vs. CD, 1.98±0.13). All data was analysed as a 2x2 factorial design with fructose+salt+fructose*salt included (general analysis of variance). Data is shown as estimated marginal means ± SEM for plasma samples and organ weights (CD: n=8, SD: n=8, FD: n=8, FSD: n=8). The data indicate that increased maternal intake of fructose in water and of salt in diet has marked effects on the dam’s metabolism. The excess energy intake as a result of increased simple sugar consumption leads to significant alterations in lipid metabolism, hepatomegaly and a shift in adipose tissue distribution. Intra-hepatic triglyceride concentrations in the enlarged livers and the possible consequences of these changes in maternal tissues on later growth and metabolism of adult offspring are currently being investigated.
Where applicable, experiments conform with Society ethical requirements