Abstract:
Objective: The present study assesses the thrifty phenotype
response of neonatal corticosterone programming to a diabetogenic
challenge in adult rats and the role of melatonin as
a deprogrammer. Methods: Neonates of both sexes, born of
healthy male and female rats maintained under standard
conditions of temperature and light, were separated and,
equal number of pups was assigned to lactating mothers. Pups
treated with either saline or corticosterone or, a combination
of corticosterone and melatonin from postnatal day (PND) 2
to PND 14 and, at 120 days of age, six animals from each treatment
group were rendered diabetic by alloxanization. Various
serum and tissue parameters pertaining to glycaemic regulation,
dyslipidemia, hepatic and renal distress and oxidative
stress were analysed in adult rats of all groups. Results: The
results indicate compromised feed efficiency, hyperglycaemia,
hypoinsulinemia, decreased glycogen content, elevated serum
and tissue lipids and serum markers of hepatic and renal stress,
together with increased lipid peroxidation, and decreased levels
of non-enzymatic and enzymatic antioxidants in corticosterone
programmed diabetic animals than in the non-programmed
diabetic rats. However, treatment with melatonin simultaneously
prevented to a significant extent the alterations in carbohydrate
and lipid metabolism and oxidative stress. Conclusions:
Melatonin is a potent deprogrammer of neonatal corticosterone
programming effects and the adult thrifty phenotype alteration
to a diabetogenic challenge.
