Insulin-stimulated glucose disposal in patients with type I (IDDM) and type II (NIDDM) diabetes mellitus.
In conclusion, there is considerable data documenting the presence of resistance to insulin-stimulated glucose uptake in patients with either IDDM or NIDDM. However, the characteristics of this metabolic abnormality are quite different in the two syndromes. In the case of IDDM the insulin resistance appears to be secondary to the state of altered carbohydrate homeostasis, is directly proportional to the severity of fasting hyperglycemia, and can be abolished by achievement of metabolic control. As a corollary, it seems reasonable to suggest that resistance to insulin-stimulated glucose uptake is not a primary defect in the pathogenesis of IDDM. Nevertheless, the presence of insulin resistance in the poorly-controlled patient with IDDM may be of great clinical relevance, and contribute to the difficulty in effective treatment of this syndrome. In contrast, resistance to insulin-stimulated glucose uptake does not seem to be a simple function of severity of hyperglycemia in patients with NIDDM, and significant insulin resistance can exist in these patients in association with only mild carbohydrate intolerance. Furthermore, although the decline in insulin-stimulated glucose disposal present in patients with significant fasting hyperglycemia can be increased by instituting excellent metabolic control with exogenous insulin, it cannot be restored to normal. These observations suggest that some component of the insulin resistance in NIDDM is similar to that in IDDM, and is secondary to the state of poor metabolic control. On the other hand, it also suggests that another component of the insulin resistance in NIDDM is primary, and most likely related to the pathogenesis of this syndrome. Obviously, there is a great need to define the mechanism of this unexplained portion of the insulin resistance of NIDDM.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000188:drug therapy; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy; D004285:Dogs; D006801:Humans; D007328:Insulin / Q000627:therapeutic use*; D007333:Insulin Resistance
D001786:Blood Glucose; D007328:Insulin