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अमूर्त

Necrotizing Enterocolitis in Rat Offspring Exposed to Placental Insufficiency: Role of Aldosterone, Oxidative Stress and Leptin

Norma B Ojeda

Background: Necrotizing enterocolitis (NEC) is a leading cause of morbidity and mortality in the neonatal intensive care unit among premature and low birth weight infants. Formula feeding, cold exposure, and altered intestinal bacterial colonization are frequently associated with this condition. However, there are few studies linking factors associated with placental function and necrotizing enterocolitis.
Aim: To investigated the role of aldosterone, oxidative stress and leptin in the development of NEC. The hypothesis proposes that Aldosterone, Oxidative Stress and Leptin are associated with development of NEC in rat offspring exposed to placental insufficiency.
Method: Premature low birth weight rat’s offspring were exposed to induced-NEC immediately after birth during 24hs. Leptin, aldosterone, and oxidative stress markers (superoxide dismutase activity, total antioxidant capacity and lipid peroxidation) were assessed at birth. Intestinal injury was evaluated after 24 hr of induced-NEC. Male and female offspring were divided in 4 groups with “n”=8, per group.
Results: Plasma levels of Aldosterone and Oxidative Stress markers were significantly greater, and leptin levels were significantly lower in premature low birth weight offspring compared to normal offspring (P<0.05). Intestinal injury was greater, and survival rate was lower in premature low birth weight offspring compared to normal offspring (P<0.05).
Conclusion: These results suggest that plasma levels of aldosterone, oxidative stress and leptin at birth are associated with the susceptibility to develop necrotizing enterocolitis in premature low birth weight offspring in a rat model of placental insufficiency.