The Interrelationship Between Cardiac Autonomic Activity and Low-Grade Inflammation in Subjects with Obesity and...

The study aimed to assess sympathetic (SNS) and parasympathetic (PSNS) activity in individuals with obesity and different states of prediabetes and to assess their associations with markers of inflammation.A total of 104 participants (mean age 46.7±10.3 years; mean body mass index (BMI) 31.5±6.3 kg/m2) were categorized into three age- and BMI-matched groups based on glucose tolerance: 1) with normal glucose tolerance (n=20); 2) with high 1-h plasma glucose > 8.6 mmol/l (n=25) 3) with impaired glucose tolerance (n=59). All participants underwent an oral glucose tolerance test, and the area under the curves for glucose, insulin, and C-peptide were calculated. Creatinine (CKD-EPI calculation), lipids, glycated haemoglobin, and inflammatory markers (C-reactive protein (CRP), serum amyloid A, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, interleukin-6 (IL-6), IL-8, and tumor necrosis factor-α) levels were measured. Body composition was assessed by bioimpedance analysis. Tissue advanced glycation end-products (AGEs) were evaluated by AGE-Reader. Autonomic function was measured with the АNX-3.0 autonomic monitoring system.A progressive decline in resting and stimulated PSNS and SNS activity was observed with worsening glucose tolerance. Some of the inflammatory markers were numerically elevated in prediabetic stages. After adjustment for age, there was a reciprocal relationship between PSNS and SNS tone and CRP (r=-0.23 to-0.40, all p<0.025). An independent inverse relationship was found between PSNS tone and systolic blood pressure and CRP. However, after adjustment for BMI and/or body composition parameters, waist circumference was the only independent predictor of PSNS activity (p<0.0001), explaining 26% of its variation.This study demonstrates an inverse relationship between PSNS activity and both systolic blood pressure and CRP levels, though this association is largely mediated by visceral obesity.