Supporting these theories, studies on rats demonstrated that rodents with VMH lesions developed signs of decreased sympathetic nervous system function and hyperinsulinemia even in the absence of hyperphagia or obesity, and pancreatic vagotomy prevented the exaggerated secretion of glucose-stimulated insulin in VMH lesioned rats; furthermore, higher-fasting insulin levels were detected among patients with HO compared with individuals with a common diet [4,39,40,41]. This evidence concerns the gene INS and hyperinsulinism.