Abstract
Background:Ethanol consumption during pregnancy can lead to a range of adverse developmental outcomes in children, termed fetal alcohol spectrum disorder (FASD). Central nervous system injury is a debilitating and widely studied manifestation of chronic prenatal ethanol exposure (CPEE). However, CPEE can also cause structural and functional deficits in metabolic pathways in offspring.Objectives and Methods:This study tested the hypothesis that CPEE increases whole-body adiposity and disrupts pancreatic structure in guinea pig offspring. Pregnant guinea pigs received ethanol (4 g kg−1 maternal body weight per day) or isocaloric-sucrose/pair-feeding (control) for 5 days per week throughout gestation.Results:Male and female CPEE offspring demonstrated growth restriction at birth, followed by a rapid period of catch-up growth before weaning (postnatal day (PD) 1–7). Whole-body magnetic resonance imaging (MRI) in young adult offspring (PD100–140) revealed increased visceral and subcutaneous adiposity produced by CPEE. At the time of killing (PD150–200), CPEE offspring also had increased pancreatic adipocyte area and decreased β-cell insulin-like immunopositive area, suggesting reduced insulin production and/or secretion from pancreatic islets.Conclusion:CPEE causes increased adiposity and pancreatic dysmorphology in offspring, which may signify increased risk for the development of metabolic syndrome and type 2 diabetes mellitus.
Highlights
Maternal alcohol consumption during pregnancy can lead to a range of adverse developmental outcomes in children, which are collectively termed fetal alcohol spectrum disorder (FASD).[1,2] Central nervous system injury is a widely studied manifestation of FASD as it is often the most debilitating and permanent consequence of prenatal ethanol exposure.[1]
Two- adipose tissue volume, such that chronic prenatal ethanol exposure (CPEE) offspring had increased way analysis of variance (ANOVA) demonstrated a significant effect of maternal treatment (F(1, 47) 1⁄4 13.91, Po0.001) on adipose tissue volume adipose tissue volume compared with sucrose control offspring (Figure 3c)
The results of the present study demonstrate that CPEE, via chronic maternal ethanol administration, causes metabolic teratogenicity in guinea pig offspring
Summary
Ethanol consumption during pregnancy can lead to a range of adverse developmental outcomes in children, termed fetal alcohol spectrum disorder (FASD). Central nervous system injury is a debilitating and widely studied manifestation of chronic prenatal ethanol exposure (CPEE). CPEE can cause structural and functional deficits in metabolic pathways in offspring. OBJECTIVES AND METHODS: This study tested the hypothesis that CPEE increases whole-body adiposity and disrupts pancreatic structure in guinea pig offspring. Whole-body magnetic resonance imaging (MRI) in young adult offspring (PD100–140) revealed increased visceral and subcutaneous adiposity produced by CPEE. At the time of killing (PD150–200), CPEE offspring had increased pancreatic adipocyte area and decreased b-cell insulin-like immunopositive area, suggesting reduced insulin production and/or secretion from pancreatic islets. CONCLUSION: CPEE causes increased adiposity and pancreatic dysmorphology in offspring, which may signify increased risk for the development of metabolic syndrome and type 2 diabetes mellitus.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
