Insulin receptors and functions in normal and spontaneously transformed cloned rat hepatocytes.

Spontaneous transformation of late passages of a cloned line of normal, differentiated, diploid rat hepatocytes (RL-PR-C) leads, not only to a loss of contact-inhibition of growth and ultimately to oncogenicity, but also to a variety of characteristics suggestive of a loss of involvement with insulin: lack of a serum requirement for growth; reductions in numbers and affinity of insulin receptors; increased rate of dissociation of insulin; loss of insulin stimulation of protein synthesis; and, a reduction in insulin's ability to activate glycogen synthase and to stimulate glycogen synthesis from glucose.