Hormonal
Exposure to the environmental contaminant tributyltin chloride (TBT) acts as a potent inducer of adipogenesis in vertebrates by functioning as a dual nanomolar-affinity ligand for retinoid X receptor (RXR) and peroxisome proliferator-activated receptor gamma (PPARγ), leading to increased lipid accumulation and adipose mass.
This research identifies a specific environmental chemical, tributyltin chloride (TBT), as a direct cause of increased fat mass in vertebrates. TBT acts by hijacking key fat-regulating receptors (RXR and PPARγ). While this does not provide a direct lifestyle intervention, it highlights that reducing exposure to organotin contaminants (found in some seafood, plastics, and treated materials) may be a relevant factor in obesity prevention strategies alongside diet and exercise.
Here we show that the persistent and ubiquitous environmental contaminant, tributyltin chloride (TBT), induces the differentiation of adipocytes in vitro and increases adipose mass in vivo. TBT is a dual, nanomolar affinity ligand for both the retinoid X receptor (RXR) and the peroxisome proliferator-activated receptor (cid:1) (PPAR(cid:1)).
Why this rating
The study uses multiple robust models (in vitro cell lines, in vivo mouse, and amphibian Xenopus) with consistent results, though it is an animal study.
Source
Endocrine-Disrupting Organotin Compounds Are Potent Inducers of Adipogenesis in Vertebrates
Felix Grün et al. · Molecular Endocrinology · 2006
DOI 10.1210/me.2005-0367
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