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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #209761
Title: Metabolic syndrome pathophysiology: the role of adipose tissue

Author
item LACLAUSTRA, MARTIN - ARAGON INST., SPAIN
item CORELLA, DOLORES - UNIV OF VALENCIA, SPAIN
item Ordovas, Jose

Submitted to: Nutrition Metabolism and Cardiovascular Disease
Publication Type: Review Article
Publication Acceptance Date: 10/20/2006
Publication Date: 2/1/2007
Citation: Laclaustra, M., Corella, D., Ordovas, J.M. 2007. Metabolic syndrome pathophysiology: the role of adipose tissue. Nutrition Metabolism and Cardiovascular Disease. 17(2):125-39.

Interpretive Summary:

Technical Abstract: Several physiopathological explanations for the metabolic syndrome have been proposed involving insulin resistance, chronic inflammation and ectopic fat accumulation following adipose tissue saturation. However, current concepts create several paradoxes, including limited cardiovascular risk reduction with intensive glucose control in diabetics, therapies that result in weight gain (PPAR agonists), and presence of some of the metabolic traits among some lipodystrophies. We propose the functional failure of an organ, in this case, the adipose tissue as a model to interpret its manifestations and to reconcile some of the apparent paradox. A cornerstone of this model is the failure of the adipose tissue to buffer postprandial lipids. In addition, homeostatic feedback loops guide physiological and pathological adipose tissue activities. Fat 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 whole body homeostasis system. These include changes in adipokines secretion and vascular effects. The functional capacity of the adipose tissue varies among subjects explaining the incomplete overlapping among the metabolic syndrome and obesity. Variations at multiple gene loci will be partially responsible for these interindividual differences. Two of those candidate genes, the adiponectin (APM1) and the perilipin (PLIN) genes are discussed in more detail.