Prä- und postprandiale Ghrelinsekretion bei Patienten mit Parkinson Erkrankung,REM-Schlaf-Verhaltensstörung und Multipler Sklerose

The secretion of the gastrointestinal hormone ghrelin is dependent on an intact vagal nerve. The discovery of pathognomonic α-synuclein aggregation in parts of the vagal nerve in earlier stages of Parkinson’s disease (PD) has led to the assumption of a potential vagal function disorder. Hypothetically this dysfunction could affect the ghrelin secretion of patients with PD and idiopathic REM-sleep behavior disorder (iRBD), a potential preclinical stage of PD. A recent study revealed an impaired postprandial ghrelin secretion in these patients. However, analysis techniques used in these studies could not distinguish between acylated and desacylated ghrelin subtypes (AG and DAG). Further investigations revealed distinct differences in their physiological effects, strongly indicating that separate measurement is required. In order to exactly determine the pathophysiological context of disturbed ghrelin secretion, the current study analyzed pre- and postprandial concentrations of AG and DAG. Additionally, patients with multiple sclerosis who also showed a change in ghrelin secretion were included. Consequently, the design of the investigation included five groups: PD patients with (n=25) and without (n=15) treatment, patients with iRBD (n=15), patients with multiple sclerosis (n=16) and healthy controls (n=25). AG and DAG were determined at eight selected points of time using a commercial “enzyme linked immunosorbent assay” (ELISA). The area under the curve, fasting concentrations of the respective hormones and the DAG:AG ratio were defined as outcome parameters. For each group of patients, we demonstrated a reduction of both AG and DAG concentrations at every measuring point. However, none of these outcome parameters reached a significant level due to a high inter-individual variability. The present results can be interpreted in two ways. Either there is no altered ghrelin secretion in the above mentioned diseases or the missing detectability is a result of an insufficient control of factors affecting AG and DAG concentrations and thus may be responsible for the high inter-individual variability. In this context, an improved preanalytic phase, a more adapted research design and objectively measured comorbidities should be considered in further research on the topic.