Fructose consumption during gestation alters glucose metabolism and placental expression of TNF‐α and SNAT2

Abstract

Increased fructose (FR) consumption has been associated with obesity and insulin resistance, which, if present during gestation, may increase the risk of metabolic disease in the offspring. Alterations in placental transport may mediate these effects. This study examined the effect of FR consumption during gestation on placental mRNA expression of nutrient transporters (GLUT3, CD36, SNAT2) and the pro‐inflammatory cytokine TNF‐α. Female rats received either 10% FR solution (n=18) or tap water (CNTL) (n=17) during gestation. Maternal blood was collected before gestation, and on gestational days (GD) 12 and 19; pregnancies were terminated on GD 20. Fetuses and placentas were weighed. Placental mRNA expression was quantified using real‐time PCR. Maternal weight, placental weight, fetal weight and GLUT3 and CD36 expression were not different between FR fed rats and CNTL rats. Maternal glucose (mmol/L) was elevated on GD 19 in FR vs. CNTL rats (6.26 ± 1.2 vs 5.18 ± 0.7; p<0.05). Insulin (ng/ml) was increased at mid‐gestation (FR: 2.74 ± 1.5; CNTL: 1.41± 0.5; p<0.05) and on GD 19 (FR: 2.11 ± 1.3; CNTL: 1.07 ± 0.4; p<0.05). Placental expression of SNAT2 (FR: 1.61 ± 0.1; CNTL: 0.90 ± 0.3; p<0.05) and TNF‐α (FR: 1.38 ± 0.2; CNTL: 0.82 ± 0.2; p<0.05) was increased in FR rats compared to CNTLs. Although overall fetal growth appeared to be unaffected, further studies examining changes in offspring metabolism are warranted. NSERC