Maternal Overconsumption of High Fructose Corn Syrup Causes Hypoxia in Placenta and Fetal Livers of Wistar Rats

Background American maternal overnutrition negatively impacts fetal development. Several epidemiological and experimental studies have demonstrated that overconsumption of diets rich in fats and sugars can have effects spanning three generations. While the negative impact of high fructose corn syrup (HFCS), a component heavily present in many processed American foods, is well‐recognized, its effects during fetal development remain largely underexplored. Thus, this study aims to examine the placental and fetal hepatic effects of HFCS maternal overconsumption. Methods Adult female Wistar rats were randomized in 2 experimental groups: HFCS Group received a 20% HFCS solution in drinking water for 30 days prior to and during pregnancy. Control Group received regular water. Prior to pregnancy, blood pressure was measured in both experimental groups by using tail‐cuff plethysmography. Fasting glucose readings were measured weekly. Terminal experiments were completed on day 21 of gestation. Placentas and fetal livers were isolated and further processed for analysis of Hypoxia‐Inducible Factor‐α (HIF‐α) expression, a classical transcription factor of hypoxia, using Western Blot. Blood samples were collected for biochemical analysis. Results Prior to pregnancy, HFCS group exhibited increased serum triglycerides (441.48 vs. 109.47 mg/dL), systolic (159.03 ± 12.04 vs. 136.29 ± 2.57 mmHg, p<0.05) and diastolic blood pressures (114.66 ± 9.47 vs. 99.29 ± 2.49 mmHg, p<0.05) compared to controls. No differences were found in glucose levels (98.17 ± 1.65 vs. 92.5 ± .24 mg/dL controls). At the terminal experimental protocol, HFCS group displayed increased HIF‐α expression in placenta (2.3 fold‐increase, p<0.05) and fetal liver (3.1 fold increase, p<0.001) compared to controls. Therefore, our results show hypoxic changes in both placental and fetal hepatic tissues. Moreover, oil red staining confirmed increased fat deposition in the maternal livers from HFCS group. Conclusion Our findings show that overconsumption of HFCS prior to and during pregnancy has a negative impact on offspring, as demonstrated by upregulation of hypoxic markers such as HIF‐α. We will further this study to determine whether other tissues undergo hypoxia and the mechanisms by which HFCS leads to hypoxia in maternal and fetal tissues. Support or Funding Information In‐house Grant NYIT This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .