ArticleToxicological sciences : an official journal of the Society of Toxicology2013
Arsenic-stimulated lipolysis and adipose remodeling is mediated by G-protein-coupled receptors.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 57 citations in OpenAlex.
- Underexplored terrain: effects of high priority environmental toxicants on skeletal muscle.Journal of toxicology and environmental health. Part B, Critical reviews · 2026Review
- Novel evidence of arsenic-related excess adiposity and its implication in the risk of cardiometabolic diseases.Environmental research · 2025Article
- Regenerative rehabilitation measures to restore tissue function after arsenic exposure.Current opinion in biomedical engineering · 2024Article
- Article
- Arsenic disrupts extracellular vesicle-mediated signaling in regenerating myofibers.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements-A Focused Review.Molecules (Basel, Switzerland) · 2022Review
- Arsenic Toxicity on Metabolism and Autophagy in Adipose and Muscle Tissues.Antioxidants (Basel, Switzerland) · 2022Review
- Is Arsenic Exposure a Risk Factor for Metabolic Syndrome? A Review of the Potential Mechanisms.Frontiers in endocrinology · 2022Review
- Developmental Exposure to Endocrine Disrupting Chemicals and Its Impact on Cardio-Metabolic-Renal Health.Frontiers in toxicology · 2021Review
- Characterization of a Coproduct from the Sea CucumberMarine drugs · 2020Article
- Arsenic Directs Stem Cell Fate by Imparting Notch Signaling Into the Extracellular Matrix Niche.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Arsenic and Obesity: a Review of Causation and Interaction.Current environmental health reports · 2020Review
- Arsenic Stimulates Myoblast Mitochondrial Epidermal Growth Factor Receptor to Impair Myogenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- A State-of-the-Science Review of Arsenic's Effects on Glucose Homeostasis in Experimental Models.Environmental health perspectives · 2020Review
- Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue.Scientific reports · 2019Article
- The role of arsenic in obesity and diabetes.Journal of cellular physiology · 2019Review
- Lipid Metabolism Alterations in a Rat Model of Chronic and Intergenerational Exposure to Arsenic.BioMed research international · 2019Article
- Regulation of cyclin D1 by arsenic and microRNA inhibits adipogenesis.Toxicology letters · 2017Article
- Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway.Scientific reports · 2016Article
- Arsenic Promotes NF-Κb-Mediated Fibroblast Dysfunction and Matrix Remodeling to Impair Muscle Stem Cell Function.Stem cells (Dayton, Ohio) · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic in drinking water promotes a number of diseases that may stem from dysfunctional adipose lipid and glucose metabolism. Arsenic inhibits adipocyte differentiation and promotes insulin resistance; however, little is known of the impacts of and mechanisms for arsenic effects on adipose lipid storage and lipolysis. Based on our earlier studies of arsenic-signaling mechanisms for vascular remodeling and inhibition of adipogenesis, we investigated the hypothesis that arsenic acts through specific adipocyte G-protein-coupled receptors (GPCRs) to promote lipolysis and decrease lipid storage. We first demonstrated that 5-week exposure of mice to 100 μg/l of arsenic in drinking water stimulated epididymal adipocyte hypertrophy, reduced the adipose tissue expression of perilipin (PLIN1, a lipid droplet coat protein), and increased perivascular ectopic fat deposition in skeletal muscle. Incubating adipocytes, differentiated from adipose-derived human mesenchymal stem cell, with arsenic stimulated lipolysis and decreased both Nile Red positive lipid droplets and PLIN1 expression. Arsenic-stimulated lipolysis was not associated with increased cAMP levels. However, preincubation of adipocytes with the Gi inhibitor, Pertussis toxin, attenuated As(III)-stimulated lipolysis and lipid droplet loss. Antagonizing Gi-coupled endothelin-1 type A and B receptors (EDNRA/EDNRB) also attenuated arsenic effects, but antagonizing other adipose Gi-coupled receptors that regulate fat metabolism was ineffective. The endothelin receptors have different roles in arsenic responses because only EDNRA inhibition prevented arsenic-stimulated lipolysis, but antagonists to either receptor protected lipid droplets and PLIN1 expression. These data support a role for specific GPCRs in arsenic signaling for aberrant lipid storage and metabolism that may contribute to the pathogenesis of metabolic disease caused by environmental arsenic exposures.
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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 Socratic graph.