ArticleMolecular endocrinology (Baltimore, Md.)2010
Prenatal exposure to the environmental obesogen tributyltin predisposes multipotent stem cells to become adipocytes.
Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 1 of them a synthesis that pooled it.
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Who cites it
135 citing papers in PubMed, 1 synthesis or guideline pooled it, 290 citations in OpenAlex.
- A systematic review of exposure to endocrine disruptors and energy expenditure in mice.Environmental health : a global access science source · 2025Pooled it
- Heritable changes in chromatin contacts associated with transgenerational susceptibility to diet-induced insulin dysregulation and obesity.Nature communications · 2026Article
- Obesity and obesity related disease in adulthood: the dark side of early life exposure to Environmental Chemical Disruptors.Journal of endocrinological investigation · 2025Review
- Tributyltin Enhances Macrophage Inflammation and Lipolysis, Contributing to Adipose Tissue Dysfunction.Journal of the Endocrine Society · 2024Article
- Placental single cell transcriptomics: Opportunities for endocrine disrupting chemical toxicology.Molecular and cellular endocrinology · 2023Article
- Environmental Health and Toxicology: Immunomodulation Promoted by Endocrine-Disrupting Chemical Tributyltin.Toxics · 2023Review
- Review
- 2,2',4,4',5,5'-Hexabromophenyl ether (BDE-153) causes abnormal insulin secretion and disorders of glucose and lipid metabolism in mice.Journal of the Chinese Medical Association : JCMA · 2023Article
- Article
- miR-223 Plays a Key Role in Obesogen-Enhanced Adipogenesis in Mesenchymal Stem Cells and in Transgenerational Obesity.Endocrinology · 2023Article
- Regulation of adipogenesis through retinoid X receptor and/or peroxisome proliferator-activated receptor by designed lignans based on natural products in 3T3-L1 cells.Journal of natural medicines · 2023Article
- 2,4-Di-tert-butylphenol Induces Adipogenesis in Human Mesenchymal Stem Cells by Activating Retinoid X Receptors.Endocrinology · 2023Article
- Perinatal exposure to tributyltin affects feeding behavior and expression of hypothalamic neuropeptide Y in the paraventricular nucleus of adult mice.Journal of anatomy · 2023Article
- Application of In Vitro Models for Studying the Mechanisms Underlying the Obesogenic Action of Endocrine-Disrupting Chemicals (EDCs) as Food Contaminants-A Review.International journal of molecular sciences · 2023Review
- Adipose-derived stem cells and obesity: The spear and shield relationship.Genes & diseases · 2023Review
- Review
- Obesity II: Establishing causal links between chemical exposures and obesity.Biochemical pharmacology · 2022Review
- Review
- Obesogens in Children-An Uncharted Territory.Metabolites · 2021Review
- PFAS and Potential Adverse Effects on Bone and Adipose Tissue Through Interactions With PPARγ.Endocrinology · 2021Review
75 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The environmental obesogen hypothesis proposes that pre- and postnatal exposure to environmental chemicals contributes to adipogenesis and the development of obesity. Tributyltin (TBT) is an agonist of both retinoid X receptor (RXR) and peroxisome proliferator-activated receptor gamma (PPARgamma). Activation of these receptors can elevate adipose mass in adult mice exposed to the chemical in utero. Here we show that TBT sensitizes human and mouse multipotent stromal stem cells derived from white adipose tissue [adipose-derived stromal stem cells (ADSCs)] to undergo adipogenesis. In vitro exposure to TBT, or the PPARgamma activator rosiglitazone increases adipogenesis, cellular lipid content, and expression of adipogenic genes. The adipogenic effects of TBT and rosiglitazone were blocked by the addition of PPARgamma antagonists, suggesting that activation of PPARgamma mediates the effect of both compounds on adipogenesis. ADSCs from mice exposed to TBT in utero showed increased adipogenic capacity and reduced osteogenic capacity with enhanced lipid accumulation in response to adipogenic induction. ADSCs retrieved from animals exposed to TBT in utero showed increased expression of PPARgamma target genes such as the early adipogenic differentiation gene marker fatty acid-binding protein 4 and hypomethylation of the promoter/enhancer region of the fatty acid-binding protein 4 locus. Hence, TBT alters the stem cell compartment by sensitizing multipotent stromal stem cells to differentiate into adipocytes, an effect that could likely increase adipose mass over time.
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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 OpenQuestion graph.