Hormonal
Exposure to environmental organotins (specifically tributyltin and triphenyltin) acts as an obesogen by functioning as nanomolar agonist ligands for nuclear receptors RXR and PPAR-gamma, thereby inappropriately driving adipocyte differentiation and increasing fat mass.
While you cannot easily control all environmental exposures, being aware that certain chemicals (like those in some plastics or treated wood) may influence fat storage biology can motivate reducing exposure where possible (e.g., avoiding plastic containers for hot foods, choosing untreated wood). However, this does not replace the fundamental importance of diet and exercise.
New data identify tributyltin chloride and triphenyltin chloride as nanomolar agonist ligands for retinoid X receptor (RXRalpha, RXRbeta, and RXRgamma) and peroxisome proliferator-activated receptor (gamma), nuclear receptors that play pivotal roles in lipid homeostasis and adipogenesis.
Why this rating
The evidence is primarily from in vitro cell cultures (3T3-L1) and animal models (mice), with human exposure levels noted but long-term causal epidemiological data in humans described as 'currently unresolved'.
Source
Environmental Obesogens: Organotins and Endocrine Disruption via Nuclear Receptor Signaling
Felix Grün et al. · Endocrinology · 2006
DOI 10.1210/en.2005-1129
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