Obesity is strongly associated to the insulin resistance syndrome, which includes type 2 diabetes mellitus, and to an increased risk of atherosclerotic cardiovascular disease [1]. Several studies have reported that visceral obesity (fat located within omental and mesenteric fat depots) is more closely associated with insulin resitance, type 2 diabetes and cardiovascular disease than is peripheral obesity (subcutaneous) [2]. However, the underlying mechanism is still unclear. Recently, a new protein Omentin 1 (also named Omentin, Intelectin-1, Endothelial Lectin HL-1 and Intestinal Lactoferrin Receptor) has been identified as a major visceral (omental) fat secretory adipokine [3]. Omentin 1 is a secreted protein of ~38kDa containing a fibrinogen-related domain that is highly expressed in the omental fat, and much less in intestine, lung and heart. Addition of recombinant Omentin 1 in vitro does not affect basal, but enhances insulin-stimulated glucose uptake in subcutaneous as well as in omental human adipocytes. Omentin 1 triggers AKT signalling in the absence of insulin [3]. Omentin 1 plasma levels measured by western blotting are decreased in obesity [4]. Omentin 1 is decreased in patients with polycystic ovary syndrome (PCOS), a disease associated with insulin resistance and obesity [5]. Glucose and Insulin negatively regulate Omentin-1 levels ex vivo and in vivo [5]. |
