Hyperglycemia-induced oxidative-stress, apoptosis, and embryopathy

Abstract

As the incidence of both type-1 and type-2 diabetes increases, more diabetes-related complications are being observed in pediatric patients. However, some diabetes-related issues in pediatric patients may be a carry-over or consequence of gestational or fetal diabetes. Elevated maternal glucose levels have been associated with increased incidence of spontaneous abortions, perinatal mortality, stillbirths, and congenital malformations. A few of these congenital malformations (embryopathy) in both humans and animals include skin discoloration; webbed toes; cleft lips and palates; congenital heart defects; and neural tube defects. While neural tube defects and congenital heart defects are the most frequent consequence of embryonic / fetal hyperglycemia, hyperglycemia-induced hepatic and renal developmental problems are also known. Hyperglycemia-induced embryopathy has been associated with reduced cell proliferation, oxidative-stress, increased rates of lipid peroxidation coupled with increased homocysteine levels, and apoptosis. Consequently, this review discusses embryonic hyperglycemia-induced reduced embryo viability, increased rates of oxidative-stress, increased lipid peroxidation rates coupled with elevated homocysteine levels, and increased apoptosis rates.