INS and hyperinsulinism: In these receptors, densely manifested in the hypothalamus, entorhinalcortex and hippocampus,43 these kinases acton insulin receptor substrates, altering metabolism and insulin signaling in thebrain, which promotes hyperinsulinemia and insulin resistance.44,45 Decreased insulin in the neurons impairsneuroplasticity, learning, and memory formation.46-48