Studies in diabetic rodents and humans provide evidence that
IGF-I may alleviate the diabetic state and
insulin resistance to some degree. To assess the efficacy of IGFs as an adjunct treatment with
insulin in diabetes, we infused
IGF-I or
des(1-3)IGF-I for 7 days at 0, 10.7, 26.7, and 66.8 nmol/day to
streptozotocin-induced diabetic rats in conjunction with infusions of 0, 2.2, 5.6, or 14 nmol/day
insulin. Both
insulin and
des(1-3)IGF-I increased
body weight gain by 7 g/day compared with controls (1.2 g/day), but there was no additive effect. However, for
nitrogen retention, the effects of
des(1-3)IGF-I were additive with those of 2.2 nmol/day
insulin.
Des(1-3)IGF-I was two- to threefold more potent than
IGF-I. At comparable rates of total
nitrogen retention, carcass
nitrogen retention was approximately 35% higher with
insulin than with IGF treatment, indicating a differential tissue response. IGFs did not alter carcass fat content.
Des(1-3)IGF-I increased
liver glycogen additively with
insulin but reduced glucosuria only when given with 5.6 nmol
insulin per day, indicating the possibility of a facilitatory effect, perhaps via increased
insulin sensitivity.
Insulin was 10- to 25-fold more potent in these glucoregulatory actions. Differential effects of the
hormones were also observed for kidney, liver, and thymus weights. We conclude that IGFs and especially the more potent
des(1-3)IGF-I may have a role as an adjunct to
insulin therapy in diabetic patients.