Endocrine Abstracts

Background: Altered signaling of hormones regulating appetite and metabolism is often observed in individuals with obesity (BMI ≥ 30 kg/m²) and related diseases, potentially resulting in increased hunger signaling and metabolic dysfunctions. Previous research indicates that such disturbances may be induced by weight gain itself, but also by other factors such as glucocorticoid excess (e.g. due to stress). However, knowledge regarding the associations between hormonal appetite signals and biological or psychological measures of stress is still limited, particularly in patients with obesity.

Methods: Data were collected from 68 patients with obesity (47 women). We assessed psychological stress perceived over the last month (via the Perceived Stress Scale (PSS)-14, ranging from 0 to 56) and biological stress (using the average of 24h urine cortisol levels of two consecutive days). In addition, we measured overnight-fasted serum levels of the hormonal appetite regulators leptin, insulin, adiponectin, FGF-21, PP, GIP, PYY, CCK and AgRP (pg/ml). To investigate cross-sectional associations between psychological/biological stress and hormonal appetite regulators, we used linear regression analysis with PSS-14 scores or urine cortisol levels as predictors, adjusted for pre-defined potential confounders (age and sex).

Results: There was a negative association between PSS-14 scores and log10-transformed FGF-21 levels (β = -0.015 (-0.028; -0.003 95% CI), P< .05) which persisted after adjustment for the potential confounders (β = -0.015 (-0.029; -0.001 95% CI), P< .05). We did not see any other associations of hormonal appetite regulators with PSS-14 scores, nor with 24h urine cortisol levels.

Conclusion: A 1-point increase on the PSS-14 score was associated with a 3.4% decrease in serum levels of the insulin sensitizer FGF-21. In patients with obesity, FGF-21 levels are often increased compared to normal weight controls, probably to compensate for metabolic challenges associated with the disease. We hypothesize that chronic stress may interfere with FGF-21 actions in these patients by decreasing FGF-21 levels; resulting in a failure to compensate for metabolic challenges. Future studies should further investigate the directionality of this association and its potential implications for eating behaviour and the development of metabolic disorders such as type 2 diabetes.