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Updated: May 22, 2026
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Tributyltin increases the expression of apoptosis- and adipogenesis-related genes in rat ovaries
Hyojin Lee1, Sojeong Lim, Sujin Yun
1Department of Bioenvironmental Technology, College of Natural Sciences, Seoul Women's University, Seoul, Korea.
Objective:
Tributyltin (TBT), an endocrine disrupting chemical, has been reported to decrease ovarian function by causing apoptosis in the ovary, but the mechanism is not fully understood. Therefore, we examined whether TBT increases the expression of adipogenesis-related genes in the ovary and the increased expression of these genes is associated with apoptosis induction.
Methods:
Three-week-old Sprague-Dawley rats were orally administered TBT (1 or 10 mg/kg body weight) or sesame oil as a control for 7 days. The ovaries were obtained and weighed on day 8, and then they were fixed for terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) or frozen for RNA extraction. Using the total RNA of the ovaries, adipogenesis- and apoptosis-related genes were analyzed by real-time polymerase chain reaction (PCR).
Results:
The ovarian weight was significantly decreased in rats administered 10 mg/kg TBT compared to that in control rats. As determined by the TUNEL assay, the number of apoptotic follicles in ovary was significantly increased in rats administered 10 mg/kg TBT. The real-time PCR results showed that the expression of adipogenesis-related genes such as PPARγ, aP2, CD36, and PEPCK was increased after TBT administration. In addition, apoptosis-related genes such as TNFα and TNFR1 were expressed more in the TBT-administered rats compared with the control rats.
Conclusion:
The present study demonstrates that TBT induces the expression of adipogenesis- and apoptosis-related genes in the ovary leading to apoptosis in the ovarian follicles. These results suggest that the increased expression of adipogenesis-related genes in the ovary by TBT exposure might induce apoptosis resulting in a loss of ovarian function.
Insights
Tributyltin (TBT) exposure increases adipogenesis and apoptosis genes in rat ovaries, leading to ovarian dysfunction. This endocrine disruptor causes ovarian follicle apoptosis, impacting reproductive health.
Area of Science:
- Endocrinology
- Toxicology
- Reproductive Biology
Background:
- Tributyltin (TBT) is an endocrine-disrupting chemical known to impair ovarian function.
- The precise mechanisms by which TBT induces ovarian apoptosis remain incompletely understood.
Purpose of the Study:
- To investigate if TBT exposure upregulates adipogenesis-related genes in the ovary.
- To determine if this upregulation is linked to TBT-induced apoptosis and subsequent loss of ovarian function.
Main Methods:
- Administration of TBT (1 or 10 mg/kg) or control (sesame oil) to Sprague-Dawley rats for 7 days.
- Ovarian weight measurement, TUNEL assay for apoptosis, and real-time PCR for gene expression analysis (adipogenesis and apoptosis markers).
Main Results:
- TBT administration (10 mg/kg) significantly reduced ovarian weight and increased ovarian follicle apoptosis.
- TBT exposure upregulated key adipogenesis genes (PPARγ, aP2, CD36, PEPCK) and apoptosis-related genes (TNFα, TNFR1).
Conclusions:
- TBT induces adipogenesis and apoptosis gene expression in ovarian follicles, leading to apoptosis.
- Increased adipogenesis gene expression by TBT exposure may drive apoptosis, contributing to ovarian dysfunction.
