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.
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.
Authors: Sander Ruiter; Josefine Sippel; Manon C Bouwmeester; Tobias Lommelaars; Piet Beekhof; Hennie M Hodemaekers; Frank Bakker; Evert-Jan van den Brandhof; Jeroen L A Pennings; Leo T M van der Ven Journal: Int J Mol Sci Date: 2016-11-02 Impact factor: 5.923