Přehled o publikaci
2024
Endocrine disruption of adipose physiology: Screening in SGBS cells
KUČERA, Jan; Zuzana CHALUPOVÁ; Martin WABITSCH and Julie DOBROVOLNÁBasic information
Original name
Endocrine disruption of adipose physiology: Screening in SGBS cells
Authors
KUČERA, Jan; Zuzana CHALUPOVÁ; Martin WABITSCH and Julie DOBROVOLNÁ
Edition
Journal of Applied Toxicology, HOBOKEN, WILEY, 2024, 0260-437X
Other information
Language
English
Type of outcome
Article in a journal
Country of publisher
United States of America
Confidentiality degree
is not subject to a state or trade secret
References:
Marked to be transferred to RIV
Yes
RIV identification code
RIV/00216224:14310/24:00137604
Organization
Přírodovědecká fakulta – Repository – Repository
UT WoS
EID Scopus
Keywords in English
adipocyte; adipogenesis; endocrine disruptors; SGBS cells; Simpson Golabi Behmel Syndrome cell line
Links
825712, interní kód Repo. 857560, interní kód Repo. RECETOX RI II, large research infrastructures.
Changed: 31/7/2025 00:50, RNDr. Daniel Jakubík
Abstract
In the original language
The increasing use of industrial chemicals has raised concerns regarding exposure to endocrine-disrupting chemicals (EDCs), which interfere with developmental, reproductive and metabolic processes. Of particular concern is their interaction with adipose tissue, a vital component of the endocrine system regulating metabolic and hormonal functions. The SGBS (Simpson Golabi Behmel Syndrome) cell line, a well-established human-relevant model for adipocyte research, closely mimics native adipocytes' properties. It responds to hormonal stimuli, undergoes adipogenesis and has been successfully used to study the impact of EDCs on adipose biology. In this study, we screened human exposure-relevant doses of various EDCs on the SGBS cell line to investigate their effects on viability, lipid accumulation and adipogenesis-related protein expression. Submicromolar doses were generally well tolerated; however, at higher doses, EDCs compromised cell viability, with cadmium chloride (CdCl2) showing the most pronounced effects. Intracellular lipid levels remained unaffected by EDCs, except for tributyltin (TBT), used as a positive control, which induced a significant increase. Analysis of adipogenesis-related protein expression revealed several effects, including downregulation of fatty acid-binding protein 4 (FABP4) by dibutyl phthalate, upregulation by CdCl2 and downregulation of perilipin 1 and FABP4 by perfluorooctanoic acid. Additionally, TBT induced dose-dependent upregulation of C/EBP alpha, perilipin 1 and FABP4 protein expression. These findings underscore the importance of employing appropriate models to study EDC-adipocyte interactions. Conclusions from this research could guide strategies to reduce the negative impacts of EDC exposure on adipose tissue.