ArticleToxicological sciences : an official journal of the Society of Toxicology2020
Gestational Cd Exposure in the CD-1 Mouse Induces Sex-Specific Hepatic Insulin Insensitivity, Obesity, and Metabolic Syndrome in Adult Female Offspring.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Endocrine-disrupting properties of heavy metal exposure contribute to the intergenerational effects on learning and memory.Frontiers in endocrinology · 2026Review
- Does consumption of a high-fructose diet during pregnancy and lactation exacerbate the effects of maternal exposure to cadmium on development and metabolic function of mouse offspring?Journal of toxicology and environmental health. Part A · 2026Article
- The effects of cadmium and high fructose diet on metabolic and reproductive health in female CD-1 mice.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025Article
- Cadmium exposure during adolescence and young adulthood induces signatures of metabolic dysfunction-associated steatotic liver disease.Scientific reports · 2025Article
- The effects of developmental cadmium exposure on health and disease.Disease models & mechanisms · 2025Review
- The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular-Kidney-Metabolic Programming.International journal of molecular sciences · 2024Review
- Obesogens: a unifying theory for the global rise in obesity.International journal of obesity (2005) · 2024Review
- Epigenetic control of the imprinted growth regulatorEpigenetics · 2023Article
- The Influence of Arsenic Co-Exposure in a Model of Alcohol-Induced Neurodegeneration in C57BL/6J Mice.Brain sciences · 2023Article
- RISING STARS: Sex differences in toxicant-associated fatty liver disease.The Journal of endocrinology · 2023Review
- Estrous cycle impacts on dendritic spine plasticity in rat nucleus accumbens core and shell and caudate-putamen.The Journal of comparative neurology · 2023Article
- Does maternal low-dose cadmium exposure increase the risk of offspring to develop metabolic syndrome and/or type 2 diabetes?Life sciences · 2023Review
- The imprinted gene Zac1 regulates steatosis in developmental cadmium-induced nonalcoholic fatty liver disease.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Perinatal Metal and Metalloid Exposures and Offspring Cardiovascular Health Risk.Current environmental health reports · 2022Review
- Estimation of Metabolic Effects upon Cadmium Exposure during Pregnancy Using Tensor Decomposition.Genes · 2022Article
- Gestational Cd Exposure in the CD-1 Mouse Sex-Specifically Disrupts Essential Metal Ion Homeostasis.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Obesity II: Establishing causal links between chemical exposures and obesity.Biochemical pharmacology · 2022Review
- Racial disparities in liver cancer: Evidence for a role of environmental contaminants and the epigenome.Frontiers in oncology · 2022Review
- Placental Gene Transcript Proportions are Altered in the Presence ofFrontiers in genetics · 2022Article
- Obesogens: How They Are Identified and Molecular Mechanisms Underlying Their Action.Frontiers in endocrinology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
There is compelling evidence that developmental exposure to toxic metals increases risk for obesity and obesity-related morbidity including cardiovascular disease and type 2 diabetes. To explore the hypothesis that developmental Cd exposure increases risk of obesity later in life, male, and female CD-1 mice were maternally exposed to 500 ppb CdCl2 in drinking water during a human gestational equivalent period (gestational day 0-postnatal day 10 [GD0-PND10]). Hallmark indicators of metabolic disruption, hepatic steatosis, and metabolic syndrome were evaluated prior to birth through adulthood. Maternal blood Cd levels were similar to those observed in human pregnancy cohorts, and Cd was undetected in adult offspring. There were no observed impacts of exposure on dams or pregnancy-related outcomes. Results of glucose and insulin tolerance testing revealed that Cd exposure impaired offspring glucose homeostasis on PND42. Exposure-related increases in circulating triglycerides and hepatic steatosis were apparent only in females. By PND120, Cd-exposed females were 30% heavier with 700% more perigonadal fat than unexposed control females. There was no evidence of dyslipidemia, steatosis, increased weight gain, nor increased adiposity in Cd-exposed male offspring. Hepatic transcriptome analysis on PND1, PND21, and PND42 revealed evidence for female-specific increases in oxidative stress and mitochondrial dysfunction with significant early disruption of retinoic acid signaling and altered insulin receptor signaling consistent with hepatic insulin sensitivity in adult females. The observed steatosis and metabolic syndrome-like phenotypes resulting from exposure to 500 ppb CdCl2 during the pre- and perinatal period of development equivalent to human gestation indicate that Cd acts developmentally as a sex-specific delayed obesogen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.