Original Communication

Journal of Neurology

, Volume 258, Issue 6, pp 982-990

First online:

Postprandial ghrelin response is reduced in patients with Parkinson’s disease and idiopathic REM sleep behaviour disorder: a peripheral biomarker for early Parkinson’s disease?

  • Marcus M. UngerAffiliated withDepartment of Neurology, Philipps-Universität Marburg Email author 
  • , Jens C. MöllerAffiliated withDepartment of Neurology, Philipps-Universität MarburgNeurocentro della Svizzera Italiana, Clinical Trials Unit, Ospedale Regionale di Lugano
  • , Katharina MankelAffiliated withDepartment of Neurology, Philipps-Universität Marburg
  • , Karla M. EggertAffiliated withDepartment of Neurology, Philipps-Universität Marburg
  • , Katharina BohneAffiliated withDivision of Gastroenterology, Philipps-University Marburg
  • , Maren BoddenAffiliated withDepartment of Neurology, Philipps-Universität Marburg
  • , Karin Stiasny-KolsterAffiliated withDepartment of Neurology, Philipps-Universität Marburg
  • , Peter H. KannAffiliated withDivision of Endocrinology and Diabetology, Philipps-University Marburg
  • , Geert MayerAffiliated withDepartment of Neurology, Hephata-Clinic Schwalmstadt-Treysa
    • , Johannes J. TebbeAffiliated withDivision of Gastroenterology, Philipps-University MarburgDeparment of Internal Medicine, Division of Gastroenterology, Klinikum Lippe
    • , Wolfgang H. OertelAffiliated withDepartment of Neurology, Philipps-Universität Marburg

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Ghrelin, an orexigenic peptide, has multiple functions, which include promoting gastrointestinal motility and influencing higher brain functions. Experimental data suggest that ghrelin has neuroprotective potential in the MPTP mouse model of Parkinson’s disease (PD). PD patients show delayed gastric emptying and other symptoms that may relate to disturbed excretion of ghrelin. No data are available on postprandial ghrelin response in patients with PD and idiopathic REM sleep behaviour disorder (iRBD)––a condition considered a putative preclinical stage of PD. We measured fasting and postprandial ghrelin serum concentrations in 20 healthy controls, 39 (including 19 drug-naïve) PD patients and 11 iRBD patients using a commercial radioimmunoassay for total ghrelin. For statistical analysis we employed ANCOVA and post-hoc testing with Bonferroni’s method. Controls showed a decrease of mean fasting ghrelin serum concentrations in the early postprandial phase, followed by a recuperation starting 60 min after the test meal and reaching a maximum at 300 min. This recuperation was less pronounced in PD and iRBD; the slope of relative postprandial ghrelin recovery was different between the investigated groups (p = 0.007). Post-hoc testing showed a difference between controls and PD patients (p = 0.002) and between controls and iRBD patients (p = 0.037). The dynamic regulation of ghrelin in response to food intake is partially impaired in subjects at putative preclinical (iRBD) and clinical stages of PD. Reduced ghrelin excretion might increase the vulnerability of nigrostriatal dopaminergic neurons as suggested by animal studies. The impaired ghrelin excretion might qualify as a peripheral biomarker and be of diagnostic or therapeutic value.


Parkinson’s disease REM sleep behaviour disorder (RBD) Ghrelin Vagal innervation, biomarker