Plasticity changes in adult metabolic homeostasis and tissue oxidative stress: neonatal programming by corticosterone and melatonin as deprogrammer

• Published in: The journal of maternal-fetal & neonatal medicine 2012-06, Vol.25 (6), p.831-844
• Main Authors: Baxi, Darshee B., Singh, Prem Kumar, Vachhrajani, Kauresh D., Ramachandran, A. V.
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Body Weight - drug effects; Body Weight - physiology; corticosterone; Corticosterone - pharmacology; diabetes; Drinking - drug effects; Drinking - physiology; Eating - drug effects; Eating - physiology; Female; Growth and Development - drug effects; Homeostasis - drug effects; Homeostasis - physiology; Male; melatonin; Melatonin - pharmacology; Metabolism - drug effects; Metabolism - physiology; neonatal; Oxidative Stress - drug effects; Oxidative Stress - physiology; Pregnancy; Rats; Rats, Wistar; stress
• ISSN: 1476-7058; 1476-4954
• DOI: 10.3109/14767058.2011.599456

Objective: To evaluate the long-term plasticity changes induced by neonatal corticosterone programming on adult metabolic status and the deprogramming effect of melatonin. Methods: Male and female Wistar rats were maintained under standard conditions and when mated females delivered pups, neonates of both sexes were separated and equal number of pups was assigned to lactating mothers. Pups treated with saline, corticosterone or a combination of corticosterone and melatonin from PND 2 to PND 14, were maintained until 120 days of age. Various serum and tissue parameters pertaining to glycaemic regulation, dyslipidemia, hepatic and renal distress and oxidative stress were analyzed in adult rats. Results: Neonatal corticosterone exposure induced dyslipidemia, increased fed and fasting glucose levels, insulin resistance, lipid peroxidation, serum levels of insulin, corticosterone and hepatic and renal dysfunction markers and decreased the levels of enzymatic and non-enzymatic antioxidants, relatively more in males. Melatonin proved as an effective deprogrammer of corticosterone induced plasticity changes. Conclusions: Neonatal corticosterone exposure induces long lasting effects on adult physiology and metabolism. Concurrent treatment with melatonin effectively deprograms the changes.