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

Authors

  • Marcus M. Unger MD,

    Corresponding author
    1. Saarland University, Department of Neurology, Homburg, Germany
    • Philipps-University Marburg, Department of Neurology, Marburg, Germany
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  • Rolf Ekman PhD, MD, BSc,

    1. The Sahlgrenska Academy at the University of Gothenburg, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Mölndal, Sweden
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  • Anna-Karin Björklund RegBS,

    1. The Sahlgrenska Academy at the University of Gothenburg, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Mölndal, Sweden
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  • Gösta Karlsson MSc,

    1. The Sahlgrenska Academy at the University of Gothenburg, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Mölndal, Sweden
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  • Chatarina Andersson RegBS,

    1. The Sahlgrenska Academy at the University of Gothenburg, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Mölndal, Sweden
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  • Katharina Mankel MD,

    1. Philipps-University Marburg, Department of Neurology, Marburg, Germany
    2. University Leipzig, Department of Visceral, Transplantation, Thoracic and Vascular Surgery, Leipzig, Germany
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  • Katharina Bohne MD,

    1. Sankt Gertrauden Krankenhaus, Department of Trauma Surgery and Orthopedy, Berlin, Germany
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  • Johannes J. Tebbe MD,

    1. Klinikum Lippe, Department of Internal Medicine, Division of Gastroenterology, Detmold, Germany
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  • Karin Stiasny-Kolster MD,

    1. Philipps-University Marburg, Department of Neurology, Marburg, Germany
    2. Somnomar, Institute for Medical Research and Sleep Medicine Marburg, Marburg, Germany
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  • Jens C. Möller MD,

    1. Philipps-University Marburg, Department of Neurology, Marburg, Germany
    2. Neurocentro della Svizzera Italiana, Ospedale Regionale di Lugano, Lugano, Switzerland
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  • Geert Mayer MD,

    1. Philipps-University Marburg, Department of Neurology, Marburg, Germany
    2. Hephata-Clinic for Neurology and Psychiatry, Schwalmstadt-Treysa, Germany
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  • Peter H. Kann PhD, MD,

    1. Philipps-University Marburg, Department of Internal Medicine, Division of Endocrinology and Diabetology, Marburg, Germany
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    • Peter H. Kann and Wolfgang H. Oertel contributed equally to the article.

  • Wolfgang H. Oertel MD

    1. Philipps-University Marburg, Department of Neurology, Marburg, Germany
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    • Peter H. Kann and Wolfgang H. Oertel contributed equally to the article.


  • Funding agencies: This work was supported by a grant from the Michael J. Fox Foundation for Parkinson's Research (to M.M.U. and W.H.O.).

  • Relevant conflicts of interest/financial disclosures: Nothing to report.

  • Full financial disclosures and author roles may be found in the online version of this article.

Correspondence to: Marcus M. Unger, MD, Department of Neurology, Saarland University, Kirrberger Strasse, 66421 Homburg, Germany; marcus.unger@uks.eu

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. © 2012 Movement Disorder Society

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