Maternal diabetes type I triggers apoptosis in the cerebellar cortex of rat offspring

Diabetes mellitus (DM) is associated with an increased risk of congenital malformations and central nervous system (CNS) disorders. This study explores the indicate the relationship between maternal type I diabetes and its specific impact on the cerebellar cortex of rat offspring, with a focus on apoptosis as a potential mechanism contributing to CNS disorders. Thirty Wistar rat dams were randomly assigned to control (CON), diabetic (STZ-D), and insulin-treated diabetic (STZ-INS) groups. The latter two are induced by a single intraperitoneal injection of streptozotocin (STZ). On postnatal day 14 (PD14), the offspring were sacrificed for assessing the numerical density of cells in the cerebellar cortex and apoptosis. The findings revealed a significant reduction in the cerebellar cortex cell count in the STZ-D group compared to the CON and STZ-INS groups (P < 0.05). Moreover, the STZ-D group exhibited a markedly higher percentage of apoptotic neurons at PD14 (P < 0.001). The primary objective of this study was to elucidate the specific impact of uncontrolled maternal diabetes on the cerebellar cortex. These findings emphasize the critical role of maternal metabolic health in neural development and shed light on the potential molecular pathways leading to adverse CNS outcomes in offspring. The study contributes novel insights to the existing body of knowledge surrounding the link between maternal diabetes and neurodevelopmental disorders, highlighting the need for targeted interventions to mitigate the impact of maternal metabolic disturbances on offspring neurobiology.