Somatic growth depends upon several factors including growth hormone (GH) and iodothyronines. The interrelationship between these two endocrine systems is very complex. Several lines of evidence suggest that triiodothyronine (T3) modulate both the pituitary secretion and peripheral actions of GH (Chernausek et al., 1983; Cabello & Wrutniak, 1989; Wolf, Ingbar & Moses, 1989; Iranmanesh et al., 1991). Studies in cultured rat pituitary cells show that T3 through binding to specific nuclear receptors both stimulates GH secretion and mRNA levels and increases insulin-like growth factor (IGF)-I receptors and IGF-I mRNA expression (Fagin, Fernandez-Mejia & Melmed, 1989; Geary et al., 1989; Matsuo et al., 1990). Since IGF-I, in turn, inhibits T3 induced GH gene expression it is speculated that the actions of T3 on GH secretion are subject to a short loop negative feedback regulation through the associated increase in pituitary IGF-I. Twentyfour- hour endogenous GH production is increased nearly fourfold in hyperthyroidism (Iranmanesh et al., 1991), whereas GH secretion and IGF-I levels are reduced in hypothyroid patients (Chernausek et al., 1983). There is also evidence to suggest that GH, in turn, influences thyroid function. GH administration in GH-deficient patients has been reported to induce a decline in circulating T4 levels and a blunting of thyroid releasing hormone (TRH) induced thyroid stimulating hormone (TSH) secretion (Root et al., 1970, 1973; Lippe et al., 1975). When combined with the relatively frequent development of clinical hypothyroidism in these patients this has led to the suggestion that GH administration suppresses thyroid function by means of a somatostatin induced supression of TSH (Lippe et al., 1975).