High Fructose Diet Modifies the Effects of Cadmium on Adverse Pregnancy Outcomes in CD-1 Mice
On this page:
Modifiable lifestyle factors, such as diet, may influence susceptibility to environmentally induced adverse pregnancy outcomes. Hence, the objective of this study was to evaluate the cumulative effects of cadmium (Cd) and high fructose diet (HFr), known hepatotoxicants, on maternal and fetal health. Female CD-1 mice were exposed to CdCl2 (0.0 ppm, 0.5 ppm, 5.0 ppm) via drinking water ± HFr (59% kcal diet) two weeks prior to breeding and through pregnancy. Maternal and fetal tissues were collected on gestation day (GD) 18 for subsequent assessments. During pregnancy, blood glucose showed Cd-mediated increases in both dietary groups at GD8 and only in the HFr group (23%) at GD18. Furthermore, mice exposed to 5.0 ppm Cd + HFr had higher HOMA-IR (p=0.09) compared to non-Cd exposed mice. Cd exposure reduced circulating T4 levels in a concentration-dependent manner. However, Cd-induced suppression of T3 was only observed in the HFr mice. Moreover, mice exposed to 5.0 ppm Cd had increased uterine arterial resistance (11%) at GD18. Despite the indication of reduced placental blood flow, fetuses from the 5.0 ppm Cd + control diet group were larger in body weight and length. Interestingly, macrosomia was not evident in the Cd + HFr groups. Our data support that Cd and HFr have independent effects on maternal and fetal health. However, the combination of these exposures contributed to hyperglycemia and thyroid hormone suppression, suggesting that HFr modifies the effects of Cd on pathways critical to the pathogenesis of adverse pregnancy outcomes. Abstract does not reflect U.S. EPA policy.