[Pathogenesis of the metabolic syndrome].
After an initial attempt by the WHO to define metabolic syndrome (MS) on a pathophysiologically oriented approach requiring the assessment of insulin resistance markers, the NCEP-ATPIII and more recently the IDF proposed more clinically oriented criteria to help, toward a preventive medicine goal, to identify patients who are likely to have features of the MS and be at increased risk of type 2 diabetes and cardio vascular disease. The notion of MS is built around abnormalities of the metabolism of lipids and carbon hydrates, a rise of blood pressure, and visceral obesity of abdominal localization. These parameters report only partially on mechanisms leading to the development of the MS. The physiopathology of MS is partially understood even today and likely results from the combination of environmental, genetic and epigenetic factors. Abdominal visceral obesity, a state of low-grade chronic inflammation and insulin resistance are the main processes susceptible to explain the various constituents of this syndrome.
Jullien
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Université Lyon 1, faculté de médecine RTH Laennec, 69288 Lyon cedex 02, France. denis.jullien@chu-lyon.fr
D004777:Environment; D015444:Exercise; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology; D007333:Insulin Resistance; D020738:Leptin / Q000502:physiology; D024821:Metabolic Syndrome / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*; D008954:Models, Biological; D009752:Nutritional Status; D011565:Psoriasis / Q000503:physiopathology*
D020738:Leptin