Abstract
Bisphenol-A (BPA) has been classified as an endocrine disruptor which disrupts normal cell function by acting as an estrogen agonist. Environmentally relevant doses of the Bisphenol-A have profound effects on rat endocrine pancreas, an essential organ involved in glucose homeostasis. Bisphenol-A acts on insulin releasing β-cells whereby it increases the pancreatic insulin content and secretion and also favours post prandial hyperinsulinemia and insulin resistance in male mice. Liver plays a central role in the control of glucose production and regulation of insulin secretion. It is one of the primary organs that are initially confronted by damage from toxic substances, xenobiotics and environmental hormones. The present study was designed to assess the effect of Bisphenol-A on insulin signal transduction and glucose oxidation in liver of adult male albino rat. Wistar strain albino rats were selected and divided into three groups, Group-I: Control, Group-II: 20mg BPA treated, Group-III: 200mg BPA treated. The IR (insulin receptor) and Akt (PKB: protein kinase B) mRNA and protein showed a decreased expression pattern in the high dose group. Eventhough there was an increase in serum insulin and a decrease in serum testosterone levels in the high dose group, the fasting blood glucose level remained unaltered. Glucose oxidation and glycogen content were found to be decreased in both high and low dose treated groups. Results of this study suggest that Bisphenol-A treatment impairs hepatic glucose oxidation and glycogen content through defective insulin signal transduction.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
