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Nuclear binding of thyroxine (T₄), cellular deiodination of T₄ and nuclear accumulation of endogenous tri-iodothyronine (T₃) were investigated in mononuclear blood cells from eight patients with anorexia nervosa.

Although the patients were euthyroid, serum T₃ was depressed and serum reverse T₃ increased. The nuclear maximal specific binding capacity (msbc) for T₄ in cells from patients with anorexia nervosa was increased (2·4 x 10^–16 mol T₄/10 µg DNA, P<0·01) as compared to that of normal subjects (msbc = 1·1 x 10^–16 mol T₄/10 µg DNA), whereas the equilibrium association constant did not differ from that of normal subjects (K_a = 2·2 x 10⁹ vs 3·0 x 10⁹l/mol).

Cellular deiodination of T₄ was significantly depressed (V_max = 4·0 x 10^–17 mol iodine/10⁶ cells per min) as compared to that of normal subjects (V_max = 2·0 x 10^–16 mol iodine/10⁶ cells per min), whereas nuclear accumulation of endogenous T₃ was normal (V_max = 3·0 10^–19 mol T₃/10 µg DNA per min).

Three patients started to gain weight and, concomitantly with the normalization of serum T₃, the nuclear T₄ capacity returned to normal. Cellular deiodination of T₄ did not normalize within the observation period.

In conclusion, patients with anorexia nervosa, in which serum T₃ is depressed, have an increased capacity of nuclear T₄ receptors. The cellular 5' deiodinase is inhibited but nuclear accumulation of endogenous T₃ is normal.