In diabetes and metabolic syndrome—where cerebrovascular reactivity and microvascular tone are impaired—such shifts could be clinically consequential: improved rCBF in prefrontal or sensorimotor hubs may secondarily improve substrate delivery (glucose, oxygen) to energetically stressed circuits, potentially aligning with the insulin-independent increases in glucose disposal observed in clamp-based experiments [158,159]. This evidence concerns the gene INS and metabolic syndrome.