Insulin-like growth factor-1 therapy in diabetes : physiologic basis, clinical benefits, and risks

To review the effects of insulin-like growth factor-1 (IGF-1) and to discuss the clinical benefits and risks of using it in patients with diabetes. Recent publications identified through a MEDLINE search using relevant keywords. Selected studies on the metabolic effects and kinetic mechanisms of in...

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Bibliographic Details
Published in:Annals of internal medicine Vol. 120; no. 1; pp. 47 - 55
Main Authors: KOLACZYNSKI, J. W, CARO, J. F
Format: Journal Article
Language:English
Published: Philadelphia, PA American College of Physicians 1994
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Summary:To review the effects of insulin-like growth factor-1 (IGF-1) and to discuss the clinical benefits and risks of using it in patients with diabetes. Recent publications identified through a MEDLINE search using relevant keywords. Selected studies on the metabolic effects and kinetic mechanisms of in vitro IGF-1 and existing literature on the effects of IGF-1 on glucose and lipid metabolism in vivo with special emphasis on data from humans. The substantial stimulatory effect of IGF-1 on glucose uptake suggests that, in selected clinical situations, the drug may be an alternative to standard treatment of diabetes. Metabolic control in patients with extreme insulin resistance is improved after using IGF-1. Moreover, patients with type II (non-insulin-dependent) diabetes who receive IGF-1 have improved glucose tolerance and decreased hyperinsulinemia and hypertriglyceridemia. The complications associated with long-term administration of IGF-1 are unknown but might include the progression of certain neoplasms and diabetic complications, such as nephropathy and retinopathy. Insulin-like growth factor-1 may be a useful adjunct for treatment of diabetes and may even be the drug of choice in some patients with extreme insulin resistance who have metabolic emergencies. However, further data are needed to evaluate the risks and benefits of IGF-1 use in diabetes and in other states associated with impaired insulin action.
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ISSN:0003-4819
1539-3704
DOI:10.7326/0003-4819-120-1-199401010-00009