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Unimpaired postprandial pancreatic polypeptide secretion in Parkinson's disease and REM sleep behavior disorder

Journal article
Authors M. M. Unger
Rolf Ekman
Anna-Karin Björklund
Gösta Karlsson
Chatarina Andersson
K. Mankel
K. Bohne
J. J. Tebbe
K. Stiasny-Kolster
J. C. Moller
G. Mayer
P. H. Kann
W. H. Oertel
Published in Movement Disorders
Volume 28
Issue 4
Pages 529-533
ISSN 0885-3185
Publication year 2013
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 529-533
Language en
Links dx.doi.org/10.1002/mds.25246
Keywords pancreatic polypeptide (PP), vagal nerve, Parkinson's disease, REM sleep behavior disorder (RBD), dopaminergic modulation, autonomic neuropathy, brain pathology, rat-brain, erythromycin, somatostatin, denervation, dysfunction, vagotomy, ghrelin
Subject categories Clinical Medicine

Abstract

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.

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