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.