Perinatal BPA Exposure Induces Hyperglycemia, Oxidative Stress and Decreased Adiponectin Production in Later Life of Male Rat Offspring

• DOI: 10.3390/ijerph110403728
• Publication Date: 2014-04-03T15:26:03Z
• Authors: Shunzhe Song; Ling Zhang; Hongyuan Zhang; Wei Wei; Lihong Jia
• Keywords: Blood Glucose; Male; 0301 basic medicine; Endocrine Disruptors; bisphenol A; glucose metabolism; adiponectin; oxidative stress; puberty stage; adult stage; Article; Rats; Rats, Sprague-Dawley; Oxidative Stress; 03 medical and health sciences; Adipose Tissue; Phenols; Pregnancy; Hyperglycemia; Prenatal Exposure Delayed Effects; Animals; Insulin; Environmental Pollutants; Female; Adiponectin; RNA, Messenger; Benzhydryl Compounds; Insulin Resistance

The main object of the present study was to explore the effect of perinatal bisphenol A (BPA) exposure on glucose metabolism in early and later life of male rat offspring, and to establish the potential mechanism of BPA-induced dysglycemia. Pregnant rats were treated with either vehicle or BPA by drinking water at concentrations of 1 and 10 µg/mL BPA from gestation day 6 through the end of lactation. We measured the levels of fasting serum glucose, insulin, adiponectin and parameters of oxidative stress on postnatal day (PND) 50 and PND100 in male offspring, and adiponectin mRNA and protein expression in adipose tissue were also examined. Our results showed that perinatal exposure to 1 or 10 µg/mL BPA induced hyperglycemia with insulin resistance on PND100, but only 10 µg/mL BPA exposure had similar effects as early as PND50. In addition, increased oxidative stress and decreased adiponectin production were also observed in BPA exposed male offspring. Our findings indicated that perinatal exposure to BPA resulted in abnormal glucose metabolism in later life of male offspring, with an earlier and more exacerbated effect at higher doses. Down-regulated expression of adiponectin gene and increased oxidative stress induced by BPA may be associated with insulin resistance.