We demonstrated dysregulation of neuroendocrine factors (NPY and leptin), proinflammatory markers (TNF-α, IL-1β, and CRP), and endothelial adhesion molecules (ICAM-1, VCAM-1, and E-selectin) in this comorbid rat model harboring metabolic and/or systemic vascular disease, plus that parallel variations may be present in patients with clinical risk factors for cerebrovascular disease. Here, SELE is linked to cerebrovascular disorder.