000148123 001__ 148123
000148123 005__ 20250114155432.0
000148123 0247_ $$2doi$$a10.1016/j.numecd.2006.10.005
000148123 0248_ $$2sideral$$a65245
000148123 037__ $$aART-2007-65245
000148123 041__ $$aeng
000148123 100__ $$aLaclaustra, M.
000148123 245__ $$aMetabolic Syndrome Pathophysiology: The Role of Adipose Tissue
000148123 260__ $$c2007
000148123 5060_ $$aAccess copy available to the general public$$fUnrestricted
000148123 5203_ $$aSeveral pathophysiological 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 overlap- ping 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
000148123 540__ $$9info:eu-repo/semantics/openAccess$$aby-nc-nd$$uhttp://creativecommons.org/licenses/by-nc-nd/3.0/es/
000148123 590__ $$a3.174$$b2007
000148123 591__ $$aCARDIAC & CARDIOVASCULAR SYSTEMS$$b17 / 75 = 0.227$$c2007$$dQ1$$eT1
000148123 591__ $$aNUTRITION & DIETETICS$$b10 / 56 = 0.179$$c2007$$dQ1$$eT1
000148123 591__ $$aENDOCRINOLOGY & METABOLISM$$b35 / 91 = 0.385$$c2007$$dQ2$$eT2
000148123 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000148123 700__ $$aCorella, D.
000148123 700__ $$aOrdovas, J. M.
000148123 773__ $$g17, 2 (2007), 125-139$$pNMCD, Nutr. Metab. Cardiovasc. Dis.$$tNutrition, Metabolism and Cardiovascular Diseases$$x0939-4753
000148123 8564_ $$s380243$$uhttps://zaguan.unizar.es/record/148123/files/texto_completo.pdf$$yVersión publicada
000148123 8564_ $$s1864929$$uhttps://zaguan.unizar.es/record/148123/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000148123 909CO $$ooai:zaguan.unizar.es:148123$$particulos$$pdriver
000148123 951__ $$a2025-01-13-14:28:13
000148123 980__ $$aARTICLE