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pubmed:abstractText |
Characteristic of both obesity and non-insulin-dependent diabetes mellitus, insulin resistance is triggered at the level of the target tissue and can be induced by three general categories of causes: (1) an abnormal beta cell secretory product, (2) circulating insulin antagonists, or (3) a target tissue defect in insulin action. Decreased numbers of insulin receptors and a post-receptor defect in insulin action both play relative roles in insulin resistance. A general trend, however, indicates that as insulin resistance increases, the post-receptor defect becomes more prominent. Impaired glucose uptake and subsequent increased hepatic glucose oxidation in non-insulin-dependent diabetes mellitus are major contributing factors to fasting hyperglycemia.
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