Publikationsserver der Universitätsbibliothek Marburg
Titel:Prä- und postprandiale Ghrelinkonzentration bei Patienten mit Multisystematrophie und Progressiver Supranukleärer Blickparese
Autor:Zoche, Lea Magdalene
Weitere Beteiligte: Ries, V. (PD Dr.)
Veröffentlicht:2018
URI:https://archiv.ub.uni-marburg.de/diss/z2018/0206
URN: urn:nbn:de:hebis:04-z2018-02066
DOI: https://doi.org/10.17192/z2018.0206
DDC:610 Medizin
Titel (trans.):Pre- and postprandial ghrelin concentration in patients with multiple system atrophy and progressive supranuclear palsy
Publikationsdatum:2018-05-03
Lizenz:https://creativecommons.org/licenses/by-nc-sa/4.0

Dokument

Schlagwörter:
Autonome Dysfunktion, autonomic dysfunction, PSP, PSP, MSA, MSA, ghrelin, Ghrelin, Multisystematrophie, Progressiver Supranukleärer Blickparese, progressive supranuclear palsy, multiple system atrophy

Zusammenfassung:
Ghrelin ist ein vorwiegend im Magen synthetisiertes Peptidhormon, welches vielfältige Funktionen im Organismus erfüllt. Besonders interessant sind neuroprotektive Eigenschaften des Hormons, die für dopaminerge Neurone in der Substantia nigra pars compacta im MPTP-Mausmodell nachgewiesen werden konnten (Andrews et al., 2009). Diese Erkenntnis macht Ghrelin für die Parkinsonforschung interessant. In einer Studie von Unger et al. (2011) konnte eine gestörte postprandiale Ghrelinsekretion bei Parkinson Patienten gezeigt werden. Aufbauend darauf wurde in dieser Arbeit das postprandiale Ghrelin-Sekretionsverhalten bei den atypischen Parkinson-Syndromen PSP und MSA untersucht. Die MSA ist neuropathologisch, wie der Morbus Parkinson eine Alpha-Synukleinopathie, während die PSP neuropathologisch zu den Tauopathien gehört. Es wurden die Serumkonzentrationen der beiden Zustandsformen, AG und DAG, bei PSP- (n=13) und MSA-Patienten (n=15) getrennt analysiert und mit einer Kontrollgruppe (n=23) verglichen. Ebenfalls wurden die AUCG, die AUCI und die Quotienten des Ghrelinabfalls und -anstiegs (Ratio 60 min/Nüchternwert und Ratio 180 min/60 min) berechnet. Wegen der kleinen Gruppengrößen wurden auch die Verhältniswerte zum jeweiligen Nüchternwert analysiert. Die Untersuchung ergab eine signifikant niedrigere Gesamtmenge von AG (AUCG) bei Patienten mit PSP im Vergleich zu gesunden Kontrollen. Auch die Relativwerte (Verhältnis zum Nüchternwert) von PSP-Patienten waren zu verschiedenen Zeitpunkten signifikant niedriger als die der Kontrollen und teilweise auch niedriger als die der MSA-Patienten. MSA Patienten und Kontrollen unterschieden sich nicht signifikant. Die genauen Regulationsmechanismen der Ghrelinsekretion sind nicht vollständig verstanden. Eine neurohumorale Kontrolle erscheint jedoch nach bisherigem Kenntnisstand wahrscheinlich. Der Einfluss des Nervus vagus ist besonders für die kephale Phase der Nahrungsaufnahme nachgewiesen, aber nicht für die postprandiale Regulation. Bei der PSP gehören autonome Funktionsstörungen bisher nicht zu den etablierten Symptomen, allerdings mehren sich Studien, die autonome Funktionsstörungen bei PSP Patienten nachweisen konnten. Anders als bei der MSA ist der Vaguskern bei der PSP nicht von einer Neurodegeneration betroffen. Es bestehen jedoch pathologische Veränderungen in einigen autonomen Zentren des Hirnstamms, die zur Erklärung autonomer Funktionsstörungen bei PSP herangezogen werden und bei der offenbar komplexen Regulation der Ghrelinspiegel involviert sein könnten.

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