Effect of Bisphenol-A on insulin signal transduction and glucose oxidation in liver of adult male albino rat

Highlights ► In our work, Bisphenol-A (BPA) treatment significantly decreased the glucose oxidation whereas the fasting blood glucose was unaffected, but decreased the glycogen concentration. ► BPA treatment resulted in hyperinsulinemia but decreased the serum testosterone. ► Levels of IR, Akt, and...

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Veröffentlicht in:	Environmental toxicology and pharmacology 2013-03, Vol.35 (2), p.300-310
Hauptverfasser:	Jayashree, Shankar, Indumathi, Dhananjayan, Akilavalli, Narasimhan, Sathish, Sampath, Selvaraj, Jayaraman, Balasubramanian, Karundevi
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Benzhydryl Compounds - toxicity Bisphenol-A Blood Glucose - analysis Cell Membrane - drug effects Cell Membrane - metabolism Cytosol - drug effects Cytosol - metabolism Emergency Endocrine disruptor Endocrine Disruptors - toxicity Glucose - metabolism Glucose Transporter Type 2 - metabolism Glycogen - metabolism Hyperinsulinemia Insulin - blood Insulin - metabolism Insulin resistance Liver - drug effects Liver - metabolism Male Oxidation-Reduction Phenols - toxicity Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Wistar Receptor, Insulin - genetics Receptor, Insulin - metabolism Signal Transduction - drug effects Testosterone - blood Xenoestrogen
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Zusammenfassung:	Highlights ► In our work, Bisphenol-A (BPA) treatment significantly decreased the glucose oxidation whereas the fasting blood glucose was unaffected, but decreased the glycogen concentration. ► BPA treatment resulted in hyperinsulinemia but decreased the serum testosterone. ► Levels of IR, Akt, and p-Akt(ser 473) proteins were impaired. ► BPA treatment significantly increased the GLUT2 mRNA as well as cytosolic and plasma membrane GLUT2 level. ► It is concluded that Bisphenol-A treatment impairs hepatic glucose oxidation through defective insulin signal transduction, but enhanced the expression of GLUT2.
ISSN:	1382-6689 1872-7077
DOI:	10.1016/j.etap.2012.12.016