IGF-1 has significant structural homology with insulin. It has been shown to bind to insulin receptors to stimulate the transport of blood sugar (glucose) into fat and muscle, inhibit excessive glucose production by the liver and lower blood glucose while simultaneously suppressing the secretion of insulin.  Studies in diabetic patients who are in insulin-deficient states have shown that their IGF-1 concentrations in the blood were also low and were increased with insulin therapy.  Similarly, administration of insulin via the portal vein (a vessel that moves blood from the spleen and gastrointestinal tract to the liver) results in optimization of plasma IGF-1 concentrations. In one study involving a patient with a partial gene deletion (a mutation in which a chromosome or a sequence of DNA is lost) of the insulin-like growth factor-1 (IGF-1) gene, Woods et al. reported that the lack of IGF-1 gene results in IGF-1 deficiency, severe insulin resistance, and short stature, and that IGF-1 therapy resulted in beneficial effects on insulin sensitivity, body composition, bone size, and linear growth.  Administration of IGF-1 in diabetic patients has also been shown to result in an improvement not only in insulin sensitivity and quality of life, but it significantly reduced the dose of the required insulin to maintain balance in glucose levels. [64-89] Taken together, these findings support that IGF-1 administration is necessary to maintain normal insulin sensitivity, and impairment in the synthesis of IGF-1 results in a worsening state of insulin resistance.
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