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Unimpaired postprandial pancreatic polypeptide secretion in Parkinson's disease and REM sleep behavior disorder
Author(s) -
Unger Marcus M.,
Ekman Rolf,
Björklund AnnaKarin,
Karlsson Gösta,
Andersson Chatarina,
Mankel Katharina,
Bohne Katharina,
Tebbe Johannes J.,
StiasnyKolster Karin,
Möller Jens C.,
Mayer Geert,
Kann Peter H.,
Oertel Wolfgang H.
Publication year - 2013
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.25246
Subject(s) - pancreatic polypeptide , postprandial , medicine , endocrinology , parkinson's disease , motilin , rem sleep behavior disorder , cholecystokinin , disease , insulin , receptor , glucagon
Background: Pancreatic polypeptide is released immediately after food ingestion. The release is operated by vagal‐abdominal projections and has therefore been suggested as a test for vagal nerve integrity. Pathoanatomical and clinical studies indicate vagal dysfunction in early Parkinson's disease (PD). Methods: We assessed the postprandial secretion of pancreatic polypeptide and motilin in healthy controls (n = 18) and patients with idiopathic rapid‐eye‐movement sleep behavior disorder (iRBD, n = 10), a potential premotor stage of PD, as well as in drug‐naive (n = 19) and treated (n = 19) PD patients. Results: The postprandial pancreatic polypeptide secretion showed a physiological pattern in all groups and even an enhanced response in drug‐naive PD and iRBD. Motilin concentrations correlated with pancreatic polypeptide concentrations. Conclusions: Postprandial pancreatic polypeptide secretion is not a suitable test for vagal nerve integrity in PD. The unimpaired pancreatic polypeptide response in iRBD and PD might be explained by partially intact vagal‐abdominal projections or compensatory mechanisms substituting a defective neuronal brain–gut axis. © 2012 Movement Disorder Society