Insulin mimics the effects of IGF-1, and vice versa [77, 78]. In the case of the

acute insulin-like effects on insulin target cells, insulin is always more potent than IGF-

1[77, 78]. Some of the insulin-like effects are mediated by a cross-reaction of the IGF-1

with the insulin receptor, but most are mediated by the IGF-1 receptor. Adipose tissue,

heart muscle, and striated muscle, typical insulin target tissue, react to IGF-1 with

increased glucose uptake [65, 77, 78, and 79]. IGF-1 usually increases glucose uptake to

the same maximum as insulin, and depending on the tissue, are 5 to 100 times less potent

than insulin [77]. In the rat heart, IGF-1 is about four to five times less potent than

insulin in stimulating glucose uptake or 3-0-methyl glucose outflow [77]. IGF-1

stimulates glucose and amino acid uptake and increases glycogen synthesis of muscle in

the same way as insulin and inhibits lipolysis of the fat cell in vitro [79]. These studies

indicate that IGF-1 may be an important regulator of glucose utilization in vivo, either

along with insulin or instead of insulin [79].

 In DM, IGF-1, which is GH dependent, is decreased in the serum of diabetic

animals and insulin dependent animals [80, 81, 82, and 83]. In diabetic swine, IGF-1

mRNA levels are decreased in heart, liver, and muscle, and this decreased gene

expression is correlated with decreased serum levels [84]. There is evidence that insulin

regulates serum IGF-1 levels by direct action on the liver and such that low insulin levels

result in low serum IGF-1 levels [81]. And in turn, low serum IGF-1 levels have been

associated with an up-regulation of IGF-1 receptors in certain tissues.

 This study will investigate whether gingival tissue demonstrates that same up-

regulation as evidenced in adipose tissue, heart muscle and striated muscle as well as

other body tissues. The study will do so by examining immunohistochemically (IHC) the