Dietary fructose during pregnancy and lactation causes enlarged livers in rat dams and impairs growth of offspring

Abstract

Maternal malnutrition is a predisposing factor for development of metabolic syndrome. Dietary fructose is linked to several metabolic disorders. We hypothesized that maternal fructose consumption would impact fetal growth and postweaning fructose intake would magnify this effect. Pregnant Sprague Dawley rats (n=27) were fed for ad‐libitum intake (AD), 30% of ad libitum intake (UN), or fed a diet containing 63% fructose (FR). Diets for AD and UN groups contained 60% carbohydrate from sucrose, corn starch and maltodextrin. Pups from UN dams weighed less (P < 0.05) at birth than AD or FR offspring (3.87 vs. 6.55 ± 0.25 g). Pups (n=107) were cross‐fostered onto dams across maternal diet groups. During lactation dams were retained on their respective gestation diets but were fed ad libitum. Pups nursed by FR dams gained 12.4% less than pups nursed by AD fed dams. At weaning male pups were fed either control diet or a diet containing 63% fructose. Liver for FR dams were 207 % of AD or UN dams (27.5 vs 13.3 g; P < 0.05). UN pups weighed less (P < 0.05) than AD or FR pups at harvest (129 d )(365.1 vs. 424.8 or 437.1 ± 8.5 g) but had greater (P < 0.05) proportion of epidydimal tissue (1.15% vs. 0.95%). In utero and suckling nutrition alter body weight, adiposity and liver mass in offspring. Fructose enlarges liver in pregnant and lactating dams. Effects of postweaning fructose are independent of maternal and suckling nutrition. NIH DK077581.