Extended Data Fig. 9: Differences in Controls based on FGF21 stress-reactivity.
From: Mitochondrial and psychosocial stress-related regulation of FGF21 in humans

(a) Controls classified as having a net positive or net negative FGF21 stress-reaction based on percent Area Under the Curve (AUC). AUC calculations were derived from baseline corrected values expressed as percent change relative to baseline FGF21, with both positive and negative peaks included in this calculation, resulting in a net percent AUC for each participant. Scatter plots show two-sided Spearmanās correlations between FGF21 reactivity and (b) cortisol reactivity (P = 0.011, n = 64), (c) cortisone reactivity (P = 0.0049, n = 55), (d) baseline testosterone levels (P = 0.019, n = 48), (e) percent body fat (P = 0.0005, n = 61), and (f) fasting insulin levels (P = 0.0069, n = 64). Reactivity for cortisol and cortisone was calculated as Percent Reactivity = ((Max_Reactivity_Value - Baseline_Value) / Baseline_Value) * 100; Baseline testosterone = measurements (pg/ml) at ā5min of the TSST time course; Fasting insulin = measurements (U/ml) at the fasting (AM) time point. Bar graphs for two-sided unpaired Mann-Whitneyās U tests with error bars representing standard error of the mean (SEM) show that Controls with positive reactivity have (b) 80% higher mean cortisol reactivity (P = 0.026, n = 44 vs 17), (c) 30% higher mean cortisone reactivity (P = 0.0023, n = 37 vs 18), and (e) 6.6% higher mean percent body fat (P = 0.0056, n = 42 vs 19). (d) Inversely, Controls with higher FGF21 reactivity had 17.61 pg/ml lower mean testosterone at baseline (P = 0.0066, n = 34 vs 14). (f) There was no statistically significant difference between high and low FGF21 reactors on baseline insulin (P = 0.16, n = 45 vs 19).