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Am J Physiol Cell Physiol. 2019 Oct 9. doi: 10.1152/ajpcell.00175.2019. [Epub ahead of print]

Bisphenol AF promotes inflammation in human white adipocytes.

Author information

1
Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX, United States.
2
Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States.

Abstract

Endocrine disrupting chemicals interact with transcription factors essential for adipocyte differentiation. Exposure to endocrine disrupting chemicals corresponds with elevated risks of obesity, but the effects of these compounds on human cells remain largely undefined. Widespread use of Bisphenol AF (BPAF) as a BPA alternative in the plastics industry presents unknown health risks. To this end, we discovered BPAF interferes with the metabolic function of mature human adipocytes. Although four-day exposures to BPAF accelerated adipocyte differentiation, we observed no effect on mature fat cell marker genes. Additional gene and protein expression analysis showed BPAF treatment during human adipocyte differentiation failed to suppress the pro-inflammatory transcription factor STAT1. Microscopy and respirometry experiments demonstrated BPAF impaired mitochondrial function and structure. To test the hypothesis that BPAF fosters vulnerabilities to STAT1 activation, we treated mature adipocytes previously exposed to BPAF with interferon gamma (IFNg). BPAF increased IFNg activation of STAT1 and exposed mitochondrial vulnerabilities that disrupt adipocyte lipid and carbohydrate metabolism. Collectively, our data establish BPAF activates inflammatory signaling pathways that degrade metabolic activity in human adipocytes. These findings suggest how the BPA alternative BPAF contributes to metabolic changes that correspond with obesity.

KEYWORDS:

PPAR gamma; adipocyte; inflammation; metabolism; transcription

PMID:
31596606
DOI:
10.1152/ajpcell.00175.2019

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