ArticleAmerican journal of physiology. Endocrinology and metabolism2020
Chronic arsenic exposure impairs adaptive thermogenesis in male C57BL/6J mice.
Article in American journal of physiology. Endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- IRF1 in Adipocytes Is Associated with Insulin Signaling and Mitochondrial Homeostasis in Diet-Induced Obesity.International journal of molecular sciences · 2026Article
- Gestational Arsenic Exposure Induces Metabolic Dysfunction-Associated Fatty Liver Disease-like Phenotypes in Middle-Aged Offspring.Environment & health (Washington, D.C.) · 2026Article
- Prenatal arsenic exposure and gene expression in fetal liver, heart, lung, and placenta.Toxicology · 2026Article
- Consensus on the key characteristics of metabolism disruptors.Nature reviews. Endocrinology · 2025Review
- Glycemic Changes Related to Arsenic Exposure: An Overview of Animal and Human Studies.Nutrients · 2024Review
- Association between Heavy Metals, Metalloids and Metabolic Syndrome: New Insights and Approaches.Toxics · 2023Review
- The pesticide chlorpyrifos promotes obesity by inhibiting diet-induced thermogenesis in brown adipose tissue.Nature communications · 2021Article
- Obesogens: How They Are Identified and Molecular Mechanisms Underlying Their Action.Frontiers in endocrinology · 2021Review
- Adipotropic effects of heavy metals and their potential role in obesity.Faculty reviews · 2021Review
- Choice of Laboratory Rodent Diet May Confound Data Interpretation and Reproducibility.Current developments in nutrition · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The global prevalence of type 2 diabetes (T2D) has doubled since 1980. Human epidemiological studies support arsenic exposure as a risk factor for T2D, although the precise mechanism is unclear. We hypothesized that chronic arsenic ingestion alters glucose homeostasis by impairing adaptive thermogenesis, i.e., body heat production in cold environments. Arsenic is a pervasive environmental contaminant, with more than 200 million people worldwide currently exposed to arsenic-contaminated drinking water. Male C57BL/6J mice exposed to sodium arsenite in drinking water at 300 μg/L for 9 wk experienced significantly decreased metabolic heat production when acclimated to chronic cold tolerance testing, as evidenced by indirect calorimetry, despite no change in physical activity. Arsenic exposure increased total fat mass and subcutaneous inguinal white adipose tissue (iWAT) mass. RNA sequencing analysis of iWAT indicated that arsenic dysregulated mitochondrial processes, including fatty acid metabolism. Western blotting in WAT confirmed that arsenic significantly decreased TOMM20, a correlate of mitochondrial abundance; PGC1A, a master regulator of mitochondrial biogenesis; and, CPT1B, the rate-limiting step of fatty acid oxidation (FAO). Our findings show that chronic arsenic exposure impacts the mitochondrial proteins of thermogenic tissues involved in energy expenditure and substrate regulation, providing novel mechanistic evidence for arsenic's role in T2D development.
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