Notably, dysglycemic states exert profound organ-specific perturbations: fetal hypoglycemia disrupts pancreatic developmental programming, hyperinsulinemic hypoglycemia reflects inherent β-cell secretory dysregulation [12], and iatrogenic hypoglycemia from exogenous insulin administration induces hepatic metabolic dysfunction coupled with aberrant expression of genes such as GLUT-1 (LC2A1), angiotensinogen (AGT), and MKP-1 (DUSP1) [13]. This evidence concerns the gene SLC2A1 and Hypoglycemia.