ArticleEnvironmental health perspectives2013
Association between arsenic suppression of adipogenesis and induction of CHOP10 via the endoplasmic reticulum stress response.
Article in Environmental health perspectives, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Association between Arsenic Exposure and Diabetes: A Meta-Analysis.BioMed research international · 2015Pooled it
- Review
- Environmental Heavy Metal Exposure and Associated Cardiovascular Diseases in Light of the Triglyceride Glucose Index.Cardiovascular toxicology · 2024Review
- Metabolic Derangement by Arsenic: a Review of the Mechanisms.Biological trace element research · 2024Review
- Metabolic Derangement by Arsenic: a Review of the Mechanisms.Biological trace element research · 2024Review
- Association between Heavy Metals, Metalloids and Metabolic Syndrome: New Insights and Approaches.Toxics · 2023Review
- Article
- Obesity II: Establishing causal links between chemical exposures and obesity.Biochemical pharmacology · 2022Review
- Arsenic Toxicity on Metabolism and Autophagy in Adipose and Muscle Tissues.Antioxidants (Basel, Switzerland) · 2022Review
- Benzene Exposure Leads to Lipodystrophy and Alters Endocrine ActivityFrontiers in endocrinology · 2022Article
- Associations between rice consumption, arsenic metabolism, and insulin resistance in adults without diabetes.International journal of hygiene and environmental health · 2021Article
- Ameliorative effect of graphene nanosheets against arsenic-induced toxicity in mice by oral exposure.Environmental science and pollution research international · 2021Article
- miR-1283 Contributes to Endoplasmic Reticulum Stress in the Development of Hypertension Through the Activating Transcription Factor-4 (ATF4)/C/EBP-Homologous Protein (CHOP) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Adipotropic effects of heavy metals and their potential role in obesity.Faculty reviews · 2021Review
- Long isoforms of NRF1 negatively regulate adipogenesis via suppression of PPARγ expression.Redox biology · 2020Article
- A State-of-the-Science Review of Arsenic's Effects on Glucose Homeostasis in Experimental Models.Environmental health perspectives · 2020Review
- Adipogenesis Regulation and Endocrine Disruptors: Emerging Insights in Obesity.BioMed research international · 2020Review
- The role of arsenic in obesity and diabetes.Journal of cellular physiology · 2019Review
- Associations of cumulative exposure to heavy metal mixtures with obesity and its comorbidities among U.S. adults in NHANES 2003-2014.Environment international · 2018Article
- Low-level arsenic causes proteotoxic stress and not oxidative stress.Toxicology and applied pharmacology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThere is growing evidence that chronic exposure to inorganic arsenic (iAs) is associated with an increased prevalence of type 2 diabetes (T2D). However, the mechanisms for the diabetogenic effect of iAs are still largely unknown. White adipose tissue (WAT) actively stores and releases energy and maintains lipid and glucose homeostasis.
objectiveWe sought to determine the mechanisms of arsenic suppression of adipogenesis.
methodsThe effects and associated mechanisms of iAs and its major metabolites on adipogenesis were determined in 3T3-L1 preadipocytes, mouse adipose-derived stromal-vascular fraction cells (ADSVFCs), and human adipose tissue-derived stem cells (ADSCs).
resultsExposure of 3T3-L1 preadipocytes to noncytotoxic levels of arsenic, including inorganic arsenite (iAs3+, ≤ 5 μM), inorganic arsenate (≤ 20 μM), trivalent monomethylated arsenic (MMA3+, ≤ 1 μM), and trivalent dimethylated arsenic (DMA3+, ≤ 2 μM) decreased adipogenic hormone-induced adipogenesis in a concentration-dependent manner. In addition, iAs3+, MMA3+, and DMA3+ exhibited a strong inhibitory effect on adipogenesis in primary cultured mouse ADSVFCs and human ADSCs. Time-course studies in 3T3-L1 cells revealed that inhibition of adipogenesis by arsenic occurred in the early stage of terminal adipogenic differentiation and was highly correlated with the induction of C/EBP homologous protein (CHOP10), an endoplasmic reticulum (ER) stress response protein. Induction of CHOP10 by arsenic is associated with reduced DNA-binding activity of CCAAT/enhancer-binding protein β (C/EBPβ), which regulates the transcription of peroxisome proliferator-activated receptor γ and C/EBPα.
conclusionsLow-level iAs and MMA3+ trigger the ER stress response and up-regulate CHOP10, which inhibits C/EBPβ transcriptional activity, thus suppressing adipogenesis. Arsenic-induced dysfunctional adipogenesis may be associated with a reduced capacity of WAT to store lipids and with insulin resistance.
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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.