Obesogens, stem cells and the maternal programming of obesity

Area of Science:

• Environmental health
• Endocrinology
• Toxicology

Background:

• Obesity and metabolic syndrome are global epidemics, often attributed to diet and inactivity.
• The environmental obesogen model suggests chemical exposures during development can influence obesity.
• Obesogens are chemicals that promote fat storage or disrupt metabolic regulation.

Purpose of the Study:

• To investigate if prenatal exposure to tributyltin (TBT), an organotin compound, influences adipogenesis and obesity risk.
• To explore the role of RXR-PPARγ signaling in TBT-induced effects on adipose tissue.

Main Methods:

• Mice were exposed to TBT during gestation (in utero).
• Assessed adipocyte differentiation, adipogenic gene expression, and overall adiposity.
• Examined the impact of TBT on the multipotent stromal cell compartment involved in fat cell development.

Main Results:

• Prenatal TBT exposure promoted adipocyte differentiation and increased adiposity in mice.
• TBT exposure altered adipogenic gene expression.
• Prenatal TBT exposure led to an increased number of preadipocytes in the multipotent stromal cell compartment.

Conclusions:

• Organotin exposure, specifically TBT, is a potential risk factor for obesity and related disorders.
• Prenatal TBT exposure may increase the number of adipocytes by altering prenatal adipose tissue development, favoring long-term obesity risk.