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The effects of cadmium exposure on maternal health are modulated by high fructose diet.
Citation:
Moore, M., H. Nguyen, F. Thomas, M. Schladweiler, D. Jenkins-Hill, A. Johnstone, L. Strader, C. Hoyo, S. Belcher, J. Dye, C. Lau, AND C. Miller. The effects of cadmium exposure on maternal health are modulated by high fructose diet. Society of Toxicology (SOT) Annual Meeting 2022, San Diego, California, March 23 - 31, 2022.
Impact/Purpose:
Exposure to pollutants rarely occurs in isolation and often co-exists with other environmental stressors. Recognizing the cumulative effects of these exposures is crucial in understanding the community-level factors that drive adverse fetal and maternal health outcomes. In this study, we investigated the interactive effects of two known hepatotoxicants—cadmium (Cd) and fructose overconsumption–on maternal health.
Description:
Exposure to pollutants rarely occurs in isolation and often co-exists with other environmental stressors. Recognizing the cumulative effects of these exposures is crucial in understanding the community-level factors that drive adverse fetal and maternal health outcomes. In this study, we investigated the interactive effects of two known hepatotoxicants—cadmium (Cd) and fructose overconsumption–on maternal health. Female CD-1 mice were exposed to Cd (0.0 ppm, 0.5 ppm, or 5.0 ppm) via drinking water ± 59% high fructose in the diet (HFrD) for two weeks prior to breeding and through gestation day (GD) 18. Bodyweight, body composition, and blood glucose were periodically monitored, and maternal tissue weights were collected at GD18. Before pregnancy, data showed that HFrD mice gained 161% more weight, had higher adiposity (fat-to-lean mass), and higher blood glucose than control diet mice. The pre-pregnancy HFrD-mediated hyperglycemia was resolved by GD8 and replaced with a CdCl2-dependent increase in blood glucose that was evident in both dietary groups. Throughout pregnancy, mice fed HFrD gained less weight than mice fed the control diet (70.2% vs. 79.2%), which resulted in a loss of the HFrD response on adiposity in non-Cd exposed dams. Nonetheless, mice exposed to 0.5 ppm Cd + HFrD maintained an elevated adiposity compared to controls. Blood glucose differences at GD8 were resolved in control diet dams, with the Cd-mediated hyperglycemia only remaining in the 5.0 ppm Cd + HFrD dams at GD18. Despite varying effects of HFrD on maternal body weight gain and body composition, HFrD intake resulted in increased kidney and liver weights at GD18. Our data support that HFrD consumption and exposure to Cd have unique effects on maternal health indices. However, the combination of these stressors results in hyperglycemia in late gestation, suggesting that a co-exposure of Cd and HFrD may impede adequate glycemic control during pregnancy. This abstract does not reflect U.S. EPA policy.