Metabolic biomarkers of appetite control in Parkinson's disease patients with and without cognitive impairment.

Background: Appetite dysregulation in Parkinson's Disease (PD) appears to be linked to physical and cognitive deterioration. PD patients with and without cognitive impairment (CI) were compared to an age-matched control group to explore predictors of appetite control in fasting and post-prandial conditions.

Methods: Fifty-five patients were recruited and divided into three groups: twenty controls (age: 74 y, BMI: 25.8 kg/m²), nineteen PD patients without CI (72.5 y, 25.1 kg/m²) and sixteen PD patients with CI (74.3 y, 24.0 kg/m²). Self-reported appetite perception and circulating blood metabolic biomarkers were measured in fasting and over a 3-h post-prandial period. Biomarkers included glucose, insulin, tumour necrosis factor alpha (TNF-α), leptin, acyl-ghrelin, total ghrelin, peptide YY (PYY), glucagon like peptide 1 (GLP-1), insulin growth factor 1 (IGF-1), growth factor (GF) and triglycerides. Patients were then provided with a mixed meal to eat ad libitum with the aim to evaluate links between metabolic biomarkers and control of energy intake.

Results: PD patients with CI had a significant lower protein intake (7.4 ± 2.5 g, p = 0.01) compared to controls (21.9 ± 3.1 g) and PD patients without CI (14.3 ± 3.0 g). Post-prandial plasma GLP-1 concentrations were associated with decreased hunger perception (B±SE, -5.3 ± 2.4  mm·h^-1, p = 0.04). PYY concentrations were significantly associated with GLP-1 in fasting (r = 0.40, p = 0.005) and post-prandial (r = 0.46, p < 0.001) conditions. In a multivariate model, post-prandial PYY concentrations were a significant predictor of ad libitum energy intake in all subjects (B±SE, -87.5 ± 34.9 kcal, p = 0.01) and in patients with PD (B±SE, -106.8 ± 44.9 kcal, p = 0.04).

Conclusions: PYY and GLP-1 appeared to influence appetite control in PD patients and their roles merit further investigation.