High Blood Glucose and Damage to Neuronal Tissue

摘要: Type-1, type-2, and gestational/embryonic diabetes are all damaging impair the nervous system. All three forms of cause oxidative stress, apoptosis, neuropathy. In type-1 type-2 (T2D), stress apoptosis involve excessive release glutamate, activation N-methyl-d-aspartate (NMDA) receptors, increased cytoplasmic Ca+2 levels, complex signaling pathways leading to apoptosis. Neuropathy has also been associated with a reduction in number neurotrophic factors, including brain-derived factor (BDNF) glial cell line-derived (GDNF), use exogenous BDNF GDNF ameliorating diabetic symptoms reported. While several regions brain affected, hypothalamus hippocampus key areas less understood, gestational causes within fetal brains embryonic hyperglycemia is hyperhomocysteinemia subsequent Elevated homocysteine (HoCys) levels promote membrane lipid peroxidation, teratogenic chicks. Data presented this review indicate that inhibits both remethylation pathway, which largely dependent on 5-methyltetrahydrofolate transsulfuration removes HoCys ultimately α-ketobutyrate, glutathione, taurine. interest because an agonist antagonist NMDA receptors.