| pubmed-article:12392600 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12392600 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:12392600 | lifeskim:mentions | umls-concept:C0011860 | lld:lifeskim |
| pubmed-article:12392600 | lifeskim:mentions | umls-concept:C0948265 | lld:lifeskim |
| pubmed-article:12392600 | lifeskim:mentions | umls-concept:C1849618 | lld:lifeskim |
| pubmed-article:12392600 | lifeskim:mentions | umls-concept:C0030012 | lld:lifeskim |
| pubmed-article:12392600 | pubmed:dateCreated | 2005-7-19 | lld:pubmed |
| pubmed-article:12392600 | pubmed:abstractText | Metabolic syndrome, insulin resistance, prediabetes, and overt type 2 diabetes mellitus are associated with an accelerated atherosclerosis (atheroscleropathy). This quartet is also associated with multiple metabolic toxicities resulting in the production of reactive oxygen species. The redox stress associated with these reactive oxygen species contribute to the development, progression, and the final fate of the arterial vessel wall in prediabetic and diabetic atheroscleropathy. The prevention of morbidity and mortality of these intersecting metabolic diseases can be approached through comprehensive global risk reduction. | lld:pubmed |
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