Abstract
The endocrine disrupting chemical, bisphenol A (BPA), has been shown to accelerate the rate of adipogenesis and increase the amount of triglyceride accumulation during differentiation of 3T3-L1 preadipocytes. The objective of this study was to investigate if that observation is mirrored in human primary cells. Here we investigated the effect of BPA on adipogenesis in cultured human primary adult stem cells. Continuous exposure to BPA throughout the 14 days of differentiation dramatically reduced triglyceride accumulation and suppressed gene transcription of the lipogenic enzyme, lipoprotein lipase (LPL). Results presented in the present study show for the first time that BPA can reduce triglyceride accumulation during adipogenesis by attenuating the expression of LPL gene transcription. Also, by employing image cytometric analysis rather than conventional Oil red O staining techniques we show that BPA regulates triglyceride accumulation in a manner which does not appear to effect adipogenesis per se.
Highlights
Adipose tissue physiology and pathophysiology is at the centre of the emerging obesity epidemic in the developed world, with much attention being paid to the role of adipose tissue dysfunction in the ever increasing incidence of metabolic diseases
Adipocytes were stained for lipid on days 0, 5, 8 and 14 of differentiation and analyzed by image cytometric software (Fig. 1A). 80 mM bisphenol A (BPA) had no significant effect on the percentage of cells that underwent adipogenic differentiation, (Fig. 1B), 80 mM BPA did significantly reduce the amount of lipid in each differentiated cell throughout maturation of adipogenesis (Fig. 1C)
Taken together these results suggest that (1) 80 mM BPA can attenuate the accumulation of lipid in differentiating adipocytes, (2) 80 mM BPA does not appear to reduce adipogenic differentiation, (3) 80 mM BPA reduces triglyceride accumulation, which appears to be independent of human Adult Stem Cells (hASCs) commitment to the adipogenic lineage
Summary
Adipose tissue physiology and pathophysiology is at the centre of the emerging obesity epidemic in the developed world, with much attention being paid to the role of adipose tissue dysfunction in the ever increasing incidence of metabolic diseases. A previous notion of adipose tissue as little more than storage depots for body energy was recently challenged with the dicovery of adiponectin [1,2,3,4], and leptin [5]. These discoveries firmly established adipose tissue as an endocrine organ and concurrently propelled adipogenesis to the forefront of scientific research. The formation of adipose tissue links the processes of adipogenesis and lipogenesis which together control both the fatcell number and size [6]. Disruption to the expression profile of either of these processes may jepardize the ability of adipose tissue to function correctly in regulating lipid metabolism and maintaining energy homeostasis
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