Hypertrophy and hyperplasia during goitre growth and involution in rats separate bioeffects of TSH and iodine

Abstract

Abstract. Goitre growth was investigated in rats receiving a low iodine diet (< 0.1 μg iodine/g) and either 1 g/l KClO4 or 1 g/l propylthiouracil (PTU), or a combination of KClO4 or PTU with 50.82 nmol/l T3 in tap water for 3 weeks. To investigate goitre involution, rats with iodine-deficient goitres were treated for 3 weeks either with T3 (0.5 μg T3/day = 0.768 nmol/day), iodide (0.5 or 2.7 μg KI/day) or a combination of T3 with both iodide doses. Histology together with total DNA distinguished between hypertrophy and hyperplasia of the gland. During goitre growth there was a highly significant correlation between goitre weight and TSH serum level (r = 0.93, P < 0.001). Thyroid total DNA, however, was only weakly correlated to TSH but was inversely related to the degree of iodine deficiency. During goitre regression, TSH levels were normalized, histological signs of hypertrophy had disappeared, and thyroid weight was nearly normalized in all therapy groups. Total DNA, however, was normalized only with 2.7 μg KI/day (95 ± 18 μg DNA/gland), and still elevated in all other groups. The highest DNA levels were found under T3 therapy (143 ± 21 μg DNA/gland) and under 0.5 μg KI/day (161 ± 19 μg DNA/gland). Reduction of total DNA was independent of TSH, but followed replenishment of the iodine content of the glands. We conclude that TSH mainly induces hypertrophy, whereas thyroid hyperplasia is mainly regulated by the intracellular iodine content.