title: Effect of bisphenol-A on insulin signal transduction and glucose oxidation in skeletal muscle of adult male albino rat.
abstract: The estrogenic monomer bisphenol-A (BPA) is an endocrine-disrupting chemical used in the production of epoxy resins, plastic food and beverage containers, leading to ubiquitous human exposure. Environmentally relevant doses of BPA have profound effects on mice endocrine pancreas. It increases pancreatic insulin content and favors postprandial hyperinsulinemia and insulin resistance in male mice. Skeletal muscle plays a crucial role in maintaining systemic glucose metabolism. In the present study, we investigated the possible effects of BPA on insulin-signaling molecules and glucose oxidation in skeletal muscle of male rat. Adult male Wistar albino rats were divided into three groups. Group I: control (vehicle treated) and groups II and III were administered with BPA orally (20 and 200 mg/kg bw/day, respectively). Although there was no change in the levels of insulin receptor (IR), Akt (protein kinase B) and glucose transporter-4 (GLUT4) messenger RNA, BPA significantly decreased the IR, Akt and GLUT4 protein levels (both plasma membrane and cytosolic fraction) of the gastrocnemius muscle. There was an increase in serum insulin and decrease in serum testosterone levels but fasting blood glucose level remained unaltered. In conclusion, BPA has adverse effects on phosphorylation of Akt, GLUT4 translocation and (14)C-glucose oxidation.
authors: Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Sekkizhar Campus, Taramani, Chennai, India.
authors: D
authors: D
authors: Indumathi
authors: S
authors: S
authors: Jayashree
authors: J
authors: J
authors: Selvaraj
authors: S
authors: S
authors: Sathish
authors: C
authors: C
authors: Mayilvanan
authors: N
authors: N
authors: Akilavalli
authors: K
authors: K
authors: Balasubramanian
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds / Q000633:toxicity*; D001786:Blood Glucose / Q000032:analysis; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000633:toxicity*; D015870:Gene Expression / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction; D010636:Phenols / Q000633:toxicity*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013739:Testosterone / Q000097:blood; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D001786:Blood Glucose; D052244:Endocrine Disruptors; D005947:Glucose; D051275:Glucose Transporter Type 4; D007328:Insulin; D010636:Phenols; D051057:Proto-Oncogene Proteins c-akt; D011972:Receptor, Insulin; D013739:Testosterone; C495694:Slc2a4 protein, rat; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: Bisphenol-A; endocrine disruptors; hyperinsulinemia; insulin resistance; skeletal muscle; testosterone