Sympathetic Overactivity, Endothelial Dysfunction, Inflammation, and Metabolic Abnormalities Cluster in Grade III (World Health Organization) Obesity

Reversal through sustained weight loss obtained with laparoscopic adjustable gastric banding

• ET-1, endothelin-1
• HOMA, homeostasis model assessment
• ICAM, intracellular adhesion molecule
• LAGB, laparoscopic adjustable gastric banding

Obesity (often complicated by type 2 diabetes), arterial hypertension, and hyperlipidemia show insulin resistance (1), metabolic abnormalities (triglycerides, insulin and blood glucose levels, and HDL cholesterol levels [2]), subclinical inflammation (3,4), functional and metabolic indexes of endothelial dysfunction (5–7), and sympathetic overactivity (8–12). Inflammation (C-reactive protein, white cells, and interleukins) is linked to metabolic abnormalities, sympathetic overactivity, and endothelial dysfunction (3,13,14).

Enlarged adipose tissue, infiltrated by macrophages, releases substances (adipokines) (15) that can explain most features of obesity (type 2 diabetes, arterial hypertension, and accelerated atherosclerosis) (16–18) including leptin, which is considered a risk factor for cardiovascular disease (19,20) and acts directly on the myocardium, stimulating cardiac hypertrophy (21,22).

Weight loss decreases the metabolic impact of obesity, reduces prevalence of type 2 diabetes and arterial hypertension (23), prevents their incidence (24,25), improves insulin resistance (26) and endothelial dysfunction (4,7), and reduces sympathetic overactivity (27), adipokines, and adhesion molecules (4,7), as well as white cells (28).

In this study, we analyzed interrelationships of metabolic abnormalities, sympathetic overactivity, inflammation, and endothelial dysfunction in obesity, including their changes induced by weight loss (laparoscopic adjustable gastric banding [LAGB]).