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Perinatal bisphenol A exposure promotes hyperactivity with corresponding hormonal responses
Author(s) -
Anderson Olivia S,
Peterson Karen E,
Sanchez Brisa N,
Zhang Zhenzhen,
Mancuso Peter,
Dolinoy Dana C
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1073.10
Subject(s) - adipokine , adiponectin , medicine , endocrinology , insulin resistance , leptin , offspring , hormone , endocrine system , insulin , obesity , pregnancy , biology , genetics
The risk of adult onset diseases is influenced by perinatal exposure to altered environmental conditions. Exposure to the endocrine active chemical, bisphenol A (BPA), has been associated with obesity and diabetes. Using an isogenic murine model, we examined perinatal exposure via maternal diet to 50 ng (n=20), 50 μg (n=21) or 50 mg (n=18) BPA/kg diet, and controls (n=20), on offspring hormones and adipokines at 9 and 10 mos of age following activity phenotyping measured at 3, 6 and 9 mos. Life‐course phenotyping revealed overall increased energy expenditure among exposed females and males (all P <0.001), and increased activity among exposed females ( P =0.06). Life‐course body composition measures did not differ in females or males (all P >;0.44), but weight and fat decreased in exposed females at particular ages (all P <0.08). At 9 mos, mg exposed females had lower baseline glucose and insulin ( P =0.05 and 0.10, respectively) indicated by an oral glucose tolerance test. Validation with homeostatic model assessment of insulin resistance indicated insulin sensitivity ( P =0.10). At 10 mos, ng and mg exposed females had increased adiponectin ( P =0.02 and 0.10, respectively). Mg exposed females had increased leptin ( P =0.10). Our life‐course phenotyping illustrates BPA exposure results in hyperactivity and corresponding hormone and adipokine responses, necessitating further evaluation of BPA as a potential obesogen. Support: MNORC P30 Center DK089503 ; NIH ES017524 ; UM P30 ES017885 Center; UM Children's Environmental Health P20 ES018171 /RD83480001 Center.