People’s Republic of ChinaIntroduction

The existence of metabolic syndrome (MetS) implies a shift from a pathophysiology concept based on metabolic abnormalities resulting from an insulin-resistant state to an epidemiological construct based on abdominal obes-ity and crude correlates of the features of insulin resist-ance. Excessive circulating adipocytokines might provide pathways linking abdominal obesity to insulin resistance, which has led several groups to try to identify secreted products derived specifically from this depot. Obestatin [1], reducing food intake, body weight gain, gastric emptying, and jejunal motility, has been demonstrated to be involved in insulin resistance and metabolic dys-functions. The functional profiles of obestatin reported in the past studies would suggest a regulator of adipo-cyte metabolism by promoting adipogenesis in an auto-crine/paracrine manner [2,3], which pointing to a putative role in the pathogenesis of metabolic syndrome. However, at present the pathophysiological role of obes-tatin in MetS remains unknown