Research

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.

ModerateSupportsMEDIUM confidence
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.
Felix Grün et al. · Endocrinology · 2006

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

narrative_reviewCited 797×
Read the paper
DOI resolved against Crossref · corpus check 2026-06-10

This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →