چکیده (انگلیسی):

Fetal/neonatal exposure to the endocrine disruptor bisphenol A (BPA) has induced obesity
and increased glucose intolerance. We hypothesized that chronic BPA exposure would
worsen the obesity and glucose intolerance induced by a high fat diet (HFD). The drinking
water of C57bl/6n dams was treated with vehicle (VEH) or BPA (25 ng/ml) from gestation
day 11.5 to postnatal day 21. Another group was treated with oral diethylstilbestrol (DES,
1 g/kg/day) during gestation. Progeny were treated with VEH (VEH and DES groups) or
BPA (2.5 ng/ml) in the drinking water and fed either a control diet (CD) or HFD from weaning
until euthanasia at 4 months of age. CD-fed mice were similar in size; however HFD-BPA
males and HFD-DES mice were smaller than HFD-VEH mice. No CD-fed mice were glucose
intolerant. All HFD-fed mice were glucose intolerant. Cholesterol and triglyceride were
increased in HFD-VEH mice and HFD-BPA males. Total fat weight and adipocyte area were
similar in HFD-VEH and HFD-BPA mice and reduced in HFD-DES mice. HFD-BPA females
increased perirenal and reduced gonadal fat weights. Reduced leptin and increased IL-6 in
CD-BPA and CD-DES mice were not found in their HFD-cohorts. Adiponectin levels were
similar. Thus, although chronic BPA exposure did not increase body size or increase glucose
intolerance, it induced an adipokine imbalance in CD-fed mice and sex-specifically altered
the lipid response and adipose deposition when fed the HFD.