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Severe thyroid hormone deficiency results in marked impairment of body growth. This is due, at least in part, to impaired growth hormone (GH) synthesis. We have studied the possible effects of severe thyroid hormone deficiency on liver receptors for GH and for prolactin (PRL) by an in vivotechnique. Female thyroidectomized (T̅) rats and age-paired controls (C) were injected iv with tracer amounts of biologically active monoiodinated hGH, alone or together with 200 μg/100 g bw of native hGH, bGH or oPRL. The liver uptake of labelled compounds, and the liver to serum radioactivity ratio was measured 20 min later. The liver to serum radioactivity ratio of C rats was decreased both by native bGH (purely somatogenic) and native oPRL (purely lactogenic). That of the T̅ rats could only decrease with bGH, Such results confirm data obtained in vitroindicating that in the severely hypothyroid rat liver there is a marked decrease in lactogenic binding and strongly suggest that specific binding of growth hormone by the liver is notsimilarly affected.