Clinical and pathophysiological consequences of abdominal adiposity and abdominal adipose tissue depots

To highlight the clinical and metabolic correlates of abdominal obesity and various abdominal adipose tissue depots.

We researched the topic using the search terms abdominal obesity, central obesity, visceral obesity, regional obesity, and subcutaneous adipose tissue from MEDLINE (National Library of Medicine, Bethesda, MD), PubMed (National Library of Medicine, Bethesda, MD), Current Contents (Institute for Scientific Information, Thomson Scientific, Philadelphia, PA), and using manual search for the cited references.

Abdominal obesity contributes significantly to the metabolic perturbations and cardiovascular risk in human beings. Abdominal adipose tissue depots (intraabdominal and subcutaneous [deep subcutaneous, posterior subcutaneous]) are metabolically active and appear to be important for the pathogenesis of insulin resistance, dyslipidemia, glucose intolerance, hypertension, hypercoagulable state, and cardiovascular risk. Adipocyte anatomy (size), physiology (growth, catecholamine sensitivity, lipolysis, insulin action), and biochemistry (leptin, plasminogen activator inhibitor-1, cytokines, renin-angiotensin system) are reported to be relatively site-specific, highlighting unique roles of regional adipose tissue depots.

Several physiological and metabolic parameters are site-specific in abdominal adipose tissue. The epidemiological, clinical, and prognostic significance and relative importance of the regional adipose tissue depots, however, remain to be ascertained.