Currently, there are no clinical studies where VIP alterations (overexpression, mutations, lack of receptors, etc.) are related with human sleep disorders. For this reason in the present section, we will be rely mention clinical studies where VIP is associated with other kind of human pathologies.
Transgenic up-regulation of expression of VIP in pancreatic islet P-cells resulted in greater secretion of insulin and improved glucose tolerance in mice (Kato et al. 1994). On the other hand, deficiencies of VIPergic nerves, assessed by morphometric criteria, have been observed on the affected tissue sites of patients with esophageal achalasia and Hirschsprung's disease of the colon, where absence of VIP may contribute to each characteristic disorder of gastrointestinal motility. Similarly, patients with cystic fibrosis or asthma have diminished respiratory airway content of VIP that may account in part for the respective abnormalities of exocrine secretion and bronchial reactivity. The absence of inactivating genetic anomalies of any of VPAC1, VPAC2, or PAC1 receptors precludes specific assignment of each neuropeptide effect to one type of receptor (Said et al. 1980; Goetzl, Adelman, and Sreedharan 1990).
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