Chronic exposure of bisphenol A impairs carbohydrate and lipid metabolism by altering corresponding enzymatic and metabolic pathways

[Display omitted] •Bisphenol-A, a widespread endocrine-disrupting chemical, has been recognized as a risk factor for metabolic disorders.•Bisphenol A impairs carbohydrate metabolism via downregulation of carbohydrate metabolizing enzymes.•Bisphenol A impairs lipid metabolism via downregulations of l...

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Veröffentlicht in:Environmental toxicology and pharmacology 2020-08, Vol.78, p.103387, Article 103387
Hauptverfasser: Haq, Muhammad Ejaz ul, Akash, Muhammad Sajid Hamid, Rehman, Kanwal, Mahmood, Malik Hassan
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Sprache:eng
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Zusammenfassung:[Display omitted] •Bisphenol-A, a widespread endocrine-disrupting chemical, has been recognized as a risk factor for metabolic disorders.•Bisphenol A impairs carbohydrate metabolism via downregulation of carbohydrate metabolizing enzymes.•Bisphenol A impairs lipid metabolism via downregulations of lipid metabolizing enzymes. Bisphenol-A (BPA), a widespread endocrine-disrupting chemical, has been recognized as a risk factor for metabolic disorders. BPA is considered to be involved in the impairment of carbohydrate and lipid metabolism but the underlying mechanisms still need to be elucidated. Present study was aimed to investigate the impact of BPA exposure on enzymatic and metabolic pathways that are responsible to regulate the carbohydrate and lipid metabolism. Experimental rats were exposed to different doses of BPA (50, 500, 2500 and 5000 μg/kg/day orally) dissolved in 1.5% dimethyl sulfoxide for a period of 3 months. Serum level of key metabolic enzymes (α-amylase, α-glucosidase, hexokinase, glucose-6-phosphatase and HMG-CoA-reductase) was measured by ELISA method. BPA-exposure suppressed the mRNA expression of gene encoding insulin resulting in poor insulin production. While hexokinase, acetyl-CoA carboxylase and squalene epoxide were up-regulated upon BPA exposure that justified the increased lipid profile. Moreover, BPA exposure showed considerably decreased glucose uptake through insulin signaling via Akt/GLUT4 pathways. There was a significant (p 
ISSN:1382-6689
1872-7077
DOI:10.1016/j.etap.2020.103387