Abstract 24: Autonomic Function and Obesity in the Coupling Between Interleukin-6 and C-Reactive Protein
C-reactive protein (CRP) is a marker of inflammation in obesity, induced in part by interleukin-6 (IL-6) derived from adipocytes. To test the hypothesis that sympathetic overactivity contributes to the increase in IL-6 and CRP, we measured these inflammatory markers in female subjects: 16 obese (42±2 yrs., BMI 37.5±1.3), 30 healthy controls (32±3 yrs., BMI 23.2±0.4), and 54 with postural tachycardia syndrome (POTS, 31±1 yrs., BMI 22.2±0.4), a condition characterized by increased sympathetic tone. We also included 3 patients with congenital absence of norepinephrine (dopamine ß-hydroxylase deficiency, DBH) as a comparison group for isolated sympathetic failure. Sympathetic activation, measured by low-frequency variability of blood pressure (LFSBP), was greater in obese and POTS compared to healthy controls (8.5±0.8 and 6.1±0.6 vs. 3.4±0.4 mmHg^2, P<0.01. Figure A). High-frequency heart rate variability (HFRRI), a marker of parasympathetic tone, was lower in POTS and in obese subjects compared to healthy controls (357±56, 402±146 and 1556±394 ms^2, respectively, P<0.01 for POTS vs. controls). IL-6 was higher in the obese and POTS groups compared to healthy controls (4.4±0.4 and 4.2±0.5 vs. 2.2±0.4 pg/mL, P<0.01. Figure B), but hsCRP was increased only in obese subjects (4.5±1.2 vs. 1.1±0.2 and 0.9±0.2 mg/L for POTS and healthy controls, P<0.01). We conclude that sympathetic activation and parasympathetic withdrawal are associated with increased serum IL-6 levels even in lean patients, but not with increased CRP. The coupling between IL-6 and CRP requires increased adiposity.
- © 2012 by American Heart Association, Inc.