Effect of type 1 diabetes during pregnancy and lactation on neonatal hypoxia‐ischemia injury and apoptotic gene expression

Abstract

AbstractObjectiveHypoxia‐ischemia (HI) is one of the major disorders that causes a variety of abnormalities and infant mortality. Type 1 diabetes is one of the most common worldwide metabolic disorders, and its prevalence has become one of the public health concerns of the 21st century. This study aims to evaluate the effect of type 1 diabetes during pregnancy and lactation on vulnerability to neonatal HI in rats.Materials and methodsFemale Wistar rats (weighing 200 ± 220 g) were randomly assigned into two groups: Group 1 (rats that received 0.5 mL/day of normal saline solution) and Group 2 (type 1 diabetes was induced in rats on the second day of pregnancy with a single dose of intraperitoneal injection of alloxan monohydrate [150 mg/kg]). After delivery, offspring were divided into four groups: (a) Control (Co), (b) Diabetic (DI), (c) Hypoxia‐ischemia (HI), (d) HI + Diabetic (HI + DI). Seven days after HI induction, neurobehavioral tests were performed, and then cerebral edema, infarct volume, inflammatory factors, Bax‐Bcl2 expression, and oxidative stress were measured.ResultsThe BAX level in the DI + HI (p = 0.0355) group was significantly higher than the HI group. The Bcl‐2 expression levels in the HI (p = 0.0027) and DI + HI (p < 0.0001) groups were significantly lower than the DI group. Total antioxidant capacity (TAC) levels in the DI + HI (p < 0.0001) group were significantly lower than HI and CO groups. TNF‐α, CRP, and total oxidant status (TOS) levels in the DI + HI (p < 0.0001) group were significantly higher than the HI group. Infarct volume and cerebral edema in the DI + HI (p < 0.0001) group were significantly higher than the HI group.ConclusionAccording to the results, type 1 diabetes during pregnancy and lactation increased the destructive effects of HI injury in pups. It also decreased the expression of the anti‐apoptotic Bcl‐2 and increased the expression BAX apoptosis factor gene in pups.