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Our results largely agree with the null hypothesis in that few time*treatment interactions were observed; prenatal undernutrition did not make the adults more susceptible to greater adipose tissue gain per se, indeed, LEL put on significantly less fat than controls when exposed to an obesogenic environment.
Thus, a variety of mechanisms, and not just a single pathway, could be involved in the observed prenatal maternal effects.
That is, the effect of prenatal exposure on the response to ethanol odor not only significantly predicts the observed prenatal effect on enhanced ethanol intake but, more importantly, a significant proportion of the enhanced ethanol intake effect can be directly attributed to the enhanced behavioral response to ethanol odor.
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It is possible that the respiratory consequences of prenatal exposure to phthalates mimic what has been observed following prenatal exposure to cigarette smoke, where several large cohort studies have essentially established its role in recurrent wheeze in very young children (Magnusson et al. 2005).
Moreover, our experimental observation corroborates previous reports on the permanent functional deficits observed after prenatal MeHg exposure.
Most importantly, very low dose rate prenatal protracted γ irradiation did not result in the same morphologic alterations in the offspring brain as previously observed after prenatal single irradiation such as derangement of the laminar structure of pyramidal cells within the hippocampus or malformation of cerebellar lobules.
Das and colleagues also observed outpatient prenatal care.
We observed that prenatal growth influences obesity characteristics, MS, IR, and stunting.
No change in striatal H-Glu uptake was observed after prenatal exposure to ethanol).
No association was observed between prenatal PCB exposure and decreased DPOAE amplitude.
Little or no association was observed for prenatal PFOA and PFOS exposure and risk of overweight.
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