Decreased insulin sensitivity (e.g. insulin resistance) is a hallmark and a major pathogenic factor of type 2 diabetes. Diabetes often is related to a cluster of arterial hypertension, obesity, impaired glucose tolerance, dyslipidemia, coagulation abnormalities, albuminuria and increased cardiovascular risk which is called metabolic syndrome. A reduction of insulin-resistance may improve metabolic syndrome, decreasing in the long term the onset of clinical diabetes and the incidence of important cardiovascular and renal complications. In the presence of insulin resistance it is altered the normal signal to the adipose tissue with a consequent reduction of absorption and use of glucose. In subjects with increased fat mass, mainly visceral, it has been shown the influence of several factors, as tumoral necrosis factor alfa (TNF alfa) and fatty free acids (FFAs), on the peripheral activity of the insulin. TNF alfa, a key modulator in fat metabolism, has a direct role on insulin-mediated homeostasis of glucose and fatty acids, regulating the action of lipoprotein lipases and fatty acid carriers influencing CoA synthesis and leptin production that, finally, inhibits insulin secretion by pancreatic beta cells. Increasing of circulating concentration of fatty acids, due to the absence of suppression of lipolysis due to insulin inactivity, contributes to peripheral and hepatic insulin resistance. It is also correlated with a condition of active inflammation, which is linked to a higher incidence of atherosclerosis and cardiovascular risk, typical of diabetes.