Hypoadiponectinemia: A link between visceral obesity and metabolic syndrome

Rosario Scaglione¹*, Tiziana Di Chiara¹, Christiano Argano², Salvatore Corrao¹ and Giuseppe Licata¹

¹Dipartimento Biomedico di Medicina Interna e Specialistica, University of Palermo, Piazza delle Cliniche 2, 90127, Palermo, Italy.

²Dipartimento di Medicina Interna, Fondazione San Raffaele Giglio, Cefalù, Palermo, Italy.

*Corresponding author. E-mail: rosarioscaglione@yahoo.It. Tel: 0916552155.

Fax: 0916552175.

Accepted 6 May, 2010

Abstract

Metabolic syndrome (MetS) represents a combination of cardio-metabolic risk factors, including visceral obesity, glucose intolerance or type 2 diabetes, elevated triglycerides, reduced HDL cholesterol, and hypertension. MetS is rapidly increasing and prevalent worldwide as a consequence of the “epidemic” obesity, with a considerable impact on the global incidence of cardiovascular disease and type 2 diabetes. At present, some authors are disappointed on the role of insulin resistance as unifying factor in the occurrence of all the MetS components, whereas the role of visceral obesity is increasing. This review summarizes and critically evaluates the clinical and scientific evidence supporting the existence of MetS as a “fatal consequence of visceral obesity”. In view of this, the effects of some adipocytokines and other proinflammatory factors produced by fat accumulation on the occurrence of the MetS have been also emphasized. Accordingly, the “hypoadiponectinemia” has been proposed as the most interesting new hypothesis to explain the pathophysiology of MetS.

Key words: Metabolic syndrome, visceral obesity, adipocytokines, adiponectin, cardiovascular disease.