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The inability to efficiently take up and store fuel, and to transition from fat to glucose as the primary source of fuel during times of plenty (increased insulin), has been termed metabolic inflexibility. This resistance to insulin is thought to be a major contributor to the whole\u2010body metabolic dysregulation that leads to increased cardiovascular risk. Recent investigation has identified specific defects in postinsulin receptor signaling in skeletal muscle from resistant humans and animals. Potential mechanisms contributing to this reduced insulin signaling and action include decreases in mitochondrial oxidative capacity, increased intramuscular lipid accumulation, increased reactive oxygen species generation, and up\u2010regulated inflammatory pathways. Future research is focused on understanding these and other potential mechanisms to identify therapeutic targets for reducing cardiometabolic syndrome risk.<\/jats:italic> <\/jats:p>","DOI":"10.1111\/j.0197-3118.2006.05455.x","type":"journal-article","created":{"date-parts":[[2007,2,7]],"date-time":"2007-02-07T15:06:08Z","timestamp":1170860768000},"page":"47-52","source":"Crossref","is-referenced-by-count":16,"title":["Skeletal Muscle Insulin Resistance Is Fundamental to the Cardiometabolic Syndrome"],"prefix":"10.1111","volume":"1","author":[{"given":"Ravi","family":"Nistala","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Craig 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