| Literature DB >> 17964909 |
Danielle Lann1, Derek LeRoith.
Abstract
Classically, the metabolic syndrome is characterized as group of pathologies including visceral obesity, hypertension, dyslipidemia, and impaired glucose tolerance. It is now realized that insulin resistance plays a principal role in initiating and perpetuating the pathologic manifestations of the metabolic syndrome. A more in-depth understanding of the basic pathophysiologic mechanisms underlying insulin resistance may aid clinicians in treating and possibly delaying or even preventing the onset of the metabolic syndrome and its complications. This article outlines how abnormal insulin signaling and secretion, impaired glucose disposal, lipotoxicity, and proinflammatory cytokines exacerbate insulin resistance and result in the perturbations of the metabolic syndrome.Entities:
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Year: 2007 PMID: 17964909 DOI: 10.1016/j.mcna.2007.06.012
Source DB: PubMed Journal: Med Clin North Am ISSN: 0025-7125 Impact factor: 5.456