A HIGH FRUCTOSE DIET AFFECTS SYNTHESIS AND COMPOSITION OF FATTY ACIDS IN THE LIVER OF LACTATING DAMS AND BODY OF THEIR SUCKLING PUPS

Abstract

Fructose (F) is a potent stimulator of hepatic lipogenesis. Long chain polyunsaturated fatty acids (LC‐PUFAs) are required during pregnancy and lactation for normal fetal and neonatal development. Despite numerous studies on F‐induced metabolic disorders in adults, the effects of dietary F on maternal and fetal lipid metabolism have not been studied. To evaluate the effects of excessive F consumption on FA synthesis, 3 groups of pregnant rats were fed isocaloric, isolipidic 60% glucose, F or starch diets from d2 of gestation to end of lactation. Compared to lactating dams fed glucose and starch, dams fed F had a 2X increase in liver mass and 4–10X increases in lipid, saturated FA, and monounsaturated FA (MUFA) content because of a dramatic rise in C16:0 and C18:1n‐9 levels. Whole body adiposity of dams was similar. Despite small increases in PUFA n‐6 and n‐3 precursors in the liver of F fed dams, C22:6n‐3 abundance was lower, suggesting that F impairs LC‐PUFA synthesis. At birth, body adiposity and fatty acid composition of pups were independent of the maternal diet. At 10 and 21 d old, % MUFA was higher in pups from F‐fed dams. During gestation, selective placental transfer of FA may shield the fetus from changes in maternal FA metabolism. After birth, the high F diet which dramatically alters maternal lipid metabolism can also alter the FA composition of the offspring, probably through FA composition in milk. (NIH‐RDK075617)