Guiding clinical decisions on abdominal obesity and cardiometabolic risk

Studies have shown that obesity increases cardiometabolic risk across the span of life. Obesity results in increased production of proinflammatory adipokines and decreased production of the anti-inflammatory adipokine, adiponectin, which eventually leads to atherosclerosis and type 2 diabetes mellitus. Lifestyle changes are the cornerstone for treatment of overweight and obese patients; however, pharmacotherapy and surgery are 2 additional treatment options that may be considered when lifestyle changes alone are unsuccessful. Adipose tissue, particularly central adipose tissue, is an endocrine organ, the actions of which tie together all components of cardiometabolic risk. Weight loss reduces levels of most proinflammatory adipokines, attenuates inflammation, improves endothelial function, and enhances insulin sensitivity. In view of these effects, obesity represents an obvious target for pharmacologic intervention. However, the benefits associated with the pharmacologic management of weight loss must be weighed against the potential for drug-related adverse events.