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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2011-1-3
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pubmed:abstractText |
Elevated blood glucose, obesity, high blood pressure, elevated triglycerides and low high density lipoprotein (HDL) cholesterol are well accepted risk factors in the development of coronary artery disease. Clustering of at least three of these factors in an individual is defined as metabolic syndrome (MetS). Obesity is a central pathological mechanism in the disease and it is expected that the incidence of this condition will increase dramatically within the next years. The visceral adipose tissue is not only an energy depot but also an endocrine organ which produces a large number of bioactive molecules, the so called adipokines. In the setting of obesity, the over-production of proinflammatory and pro-thrombotic adipokines is associated with insulin resistance. This mechanism represents the pathophysiological basis for the development of MetS. Inflammation has a central role in the pathogenesis of MetS and in mediating its impact on the development of cardiovascular disease. Knowledge of these mechanisms has relevance in the context of preventive and therapeutic strategies.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adiponectin,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensinogen,
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/CCL2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Plasminogen Activator Inhibitor 1,
http://linkedlifedata.com/resource/pubmed/chemical/Resistin,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:issn |
1093-4715
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1663-74
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pubmed:meshHeading |
pubmed-meshheading:21196255-Adiponectin,
pubmed-meshheading:21196255-Adolescent,
pubmed-meshheading:21196255-Adult,
pubmed-meshheading:21196255-Angiotensinogen,
pubmed-meshheading:21196255-Atherosclerosis,
pubmed-meshheading:21196255-Biological Markers,
pubmed-meshheading:21196255-Cardiovascular Diseases,
pubmed-meshheading:21196255-Chemokine CCL2,
pubmed-meshheading:21196255-Endothelium, Vascular,
pubmed-meshheading:21196255-Humans,
pubmed-meshheading:21196255-Inflammation,
pubmed-meshheading:21196255-Insulin Resistance,
pubmed-meshheading:21196255-Interleukin-6,
pubmed-meshheading:21196255-Intra-Abdominal Fat,
pubmed-meshheading:21196255-Leptin,
pubmed-meshheading:21196255-Life Style,
pubmed-meshheading:21196255-Metabolic Syndrome X,
pubmed-meshheading:21196255-Obesity,
pubmed-meshheading:21196255-Plaque, Atherosclerotic,
pubmed-meshheading:21196255-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:21196255-Prognosis,
pubmed-meshheading:21196255-Resistin,
pubmed-meshheading:21196255-Risk,
pubmed-meshheading:21196255-Tumor Necrosis Factor-alpha
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pubmed:year |
2011
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pubmed:articleTitle |
Inflammatory markers and cardiovascular risk in the metabolic syndrome.
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pubmed:affiliation |
2nd Department of Internal Medicine, University Medical Center of the Johannes, Gutenberg-University Mainz, Germany. espinola@uni-mainz.de
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pubmed:publicationType |
Journal Article,
Review
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