Maternal antioxidants prevent β‐cell apoptosis and promote formation of dual hormone‐expressing endocrine cells in male offspring following fetal and neonatal nicotine exposure
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AbstractBackground: Fetal and neonatal nicotine exposure causes β‐cell oxidative stress and apoptosis in neonates, leading to adult‐onset dysglycemia. The aim of the present study was to determine whether an antioxidant intervention could prevent nicotine‐induced β‐cell loss.Methods: Nulliparous female Wistar rats received daily subcutaneous injections of either saline or nicotine bitartrate (1.0 mg/kg per day) for 2 weeks prior to mating until weaning. Nicotine‐exposed dams received either normal chow or diet containing antioxidants (1000 IU/kg vitamin E, 0.25% w/w coenzyme Q10, and 0.1% w/w α‐lipoic acid) during mating, pregnancy, and lactation; saline‐exposed dams received normal chow. Pancreatic tissue was collected from male offspring at 3 weeks of age to measure β‐cell fraction, apoptosis, proliferation, and the presence of cells coexpressing insulin and glucagon.Results: The birth weight of offspring born to nicotine‐exposed dams was significantly reduced in those receiving dietary antioxidants compared with those fed normal chow. Most interestingly, the antioxidant intervention to nicotine‐exposed dams prevented the β‐cell loss and apoptosis observed in nicotine‐exposed male offspring whose mothers did not receive antioxidants. Male pups born to nicotine‐treated mothers receiving antioxidants also had a tendency for increased β‐cell proliferation and a significant increase in islets containing insulin/glucagon bihormonal cells compared with the other two treatment groups.Conclusion: The present study demonstrates that exposure to maternal antioxidants protects developing β‐cells from the damaging effects of nicotine, thus preserving β‐cell mass.
