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Reprod Toxicol. 2019 Apr;85:110-122. doi: 10.1016/j.reprotox.2019.03.002. Epub 2019 Mar 7.

Developmental programming: Changes in mediators of insulin sensitivity in prenatal bisphenol A-treated female sheep.

Author information

1
Departments of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA.
2
Departments of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
3
Departments of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA; Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
4
Departments of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA; Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: vasantha@umich.edu.

Abstract

Developmental exposure to endocrine disruptor bisphenol A (BPA) is associated with metabolic defects during adulthood. In sheep, prenatal BPA treatment causes insulin resistance (IR) and adipocyte hypertrophy in the female offspring. To determine if changes in insulin sensitivity mediators (increase in inflammation, oxidative stress, and lipotoxicity and/or decrease in adiponectin) and the intracrine steroidal milieu contributes to these metabolic perturbations, metabolic tissues collected from 21-month-old female offspring born to mothers treated with 0, 0.05, 0.5, or 5 mg/kg/day of BPA were studied. Findings showed prenatal BPA in non-monotonic manner (1) increased oxidative stress; (2) induced lipotoxicity in liver and muscle; and (3) increased aromatase and estrogen receptor expression in visceral adipose tissues. These changes are generally associated with the development of peripheral and tissue level IR and may explain the IR status and adipocyte hypertrophy observed in prenatal BPA-treated female sheep.

KEYWORDS:

Bisphenol A; Endocrine disruptor; Inflammation; Insulin resistance; Lipotoxicity; Oxidative stress

PMID:
30853570
PMCID:
PMC6443435
[Available on 2020-04-01]
DOI:
10.1016/j.reprotox.2019.03.002

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