Background: The causal factors of obesity are multi-factorial and one suggested contribution is dysregulation of appetite and satiety stimulating hormones. Peptide YY3-36 (PYY3-36) has a meal-terminating role and is proposed to be deficient in obese persons. Furthermore, obese persons have a higher prevalence of binge eating disorder (BED) of which the causality is complex. The aim of this thesis was to identify the possible associations between PYY3-36, obesity related risk factors and BED.
Subjects and methods: Through the cross-sectional melanocortin 4 receptor (MC4R) study carried out at the Department of Preventive Cardiology between 2005 and 2010, a total of 882 subjects with body mass index (BMI) ≥ 30 kg/m2 were recruited. The current study is limited to 315 subjects (62 % women), aged 18-65 years with a BMI of ≥ 40 kg/m2. Anthropometrics and blood pressure were recorded and blood samples were analyzed to obtain fasting and 2-hour post challenge glucose, glycated hemoglobin (Hba1c), fasting insulin, lipid profiles (total cholesterol, high density lipoprotein cholesterol [HDL-C], low density lipoprotein cholesterol [LDL-C], triglycerides and apo-lipoprotein B), inflammation markers (C-reactive protein [CRP] and ferritin) and fasting and post-glucose challenge PYY3-36. The Homeostasis Model Assessment 2 (HOMA2) was used to estimate insulin sensitivity (HOMA-S), steady state beta cell function (HOMA-ß) and insulin resistance (HOMA-IR). Self-administered questionnaires and the binge eating scale (BES) were completed to obtain demographic characteristics and screen for binge eating. Correlations between PYY3-36, the BES and selected variables were explored. Multiple regression and binary logistic regression were performed in models adjusted for age, sex and selected variables.
Results: Fasting and post-glucose challenge PYY3-36 concentrations were strongly correlated (p < 0.001). Unadjusted, significant correlations were found between waist circumference, systolic blood pressure (SBP) and fasting PYY3-36 (R = 0.12, p = 0.040 and R = 0.20, p = 0.001, respectively). In women, body fat percent and fasting glucose were also positively correlated to fasting PYY3-36 in an unadjusted model (R = 0.19, p = 0.012 and R = 0.16, p = 0.025, respectively). The positive correlations between body fat percent, SBP, fasting glucose and fasting PYY3-36 remained after being adjusted for age and sex. When additionally adjusted for all other variables in the model the correlation between body fat percent and fasting PYY3-36 was weaker, but still statistically significant (p = 0.025). SBP was positively correlated to PYY3-36 in the same model (p < 0.001). The BES categories were significantly, negatively correlated with age, SBP and ferritin (R = -0.11, p = 0.050; R = -0.15, p = 0.011; R = -0.16, p = 0.006, respectively). A positive, significant correlation was found between body fat percent and the BES categories (R = 0.13, p = 0.035). In men exclusively, HOMA-ß was found to be positively correlated to the BES categories (R = 0.23, P = 0.027). In an age-adjusted logistic regression model, sex and SBP were associated with binge eating(OR = 3.10, CI [1.70, 5.65], OR = 0.70, CI [0.54, 0.89]). However, when additionally adjusted for other variables in the model, only sex remained significantly associated to binge eating (OR = 3.49, CI [1.67, 7.26]).
Conclusion: Fasting PYY3-36 concentrations were independently associated with body fat percent and SBP in our population. Due to the cross-sectional design, causality cannot be assumed. Except for sex, no other variables were associated with binge eating in our study.