[Adipokines and lipids].

Insulin resistance, hyperleptinaemia and low plasma levels of adiponectin are also widely related to features of the MS. The functional capacity of the adipose tissue varies among subjects explaining the incomplete overlapping among the metabolic syndrome and obesity. Far turnover is determined by a complex equilibrium in which insulin is a main factor but not the only one. Chronically inadequate energy balance may be a key factor, stressing the system. In this situation, an adipose tissue functional failure occurs resulting in changes in systemic energy delivery, impaired glucose consumption and activation of self-regulatory mechanisms that extend their influence to the whole body homeostasis system. Lipid metabolism alterations in liver and peripheral tissues are addressed, with particular reference to adipose and muscle tissues, and the mechanisms by which some adipokines, namely leptin and adiponectin, mediate the regulation of fatty acid oxidation in those tissues. The activation of the AMPK (AMP-dependent kinase) pathway, together with a subsequent increase in the fatty acid oxidation, appear to constitute the main mechanism of action of these hormones in the regulation of lipid metabolism. A decreased activation of AMPK appears to have a role in the development of features of the MS. In addition, the alteration of AMPK signalling in the hypothalamus, which may function as a sensor of nutrient availability, integrating multiple nutritional and hormonal signals, may have a key role in the appearance of the MS.