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The purpose of this study was to investigate the effects of hyper- and hypothyroidism on thyroid hormone concentrations and deiodinase activities in nine regions of the rat brain. Four weeks of treatment with 75 microg thyroxine (T4)/kg body wt induced a two- to threefold increase in T4 levels in all of these brain regions, whereas the 3,5,3'-triiodothyronine (T3) concentrations were reduced in five brain regions and remained unchanged in four. Even after 8 wk treatment with 300 microg T4/kg, the T3 concentrations remained normal in cortical areas, the hippocampus and amygdala, and were elevated only in areas in which inner-ring deiodinase activity was low or absent, and in the hypothalamus. At the subcellular level, nuclear concentrations of T3 were diminished in hypothyroidism but remained unaltered in hyperthyroidism in all areas except the hypothalamus, where they were enhanced. Cortical mitochondrial succinate dehydrogenase activity was reduced in both hypo- and hyperthyroidism in spite of normal T3 concentrations in hyperthyroid animals. The results show that nuclear T3 concentrations fall in hypothyroidism but do not change during severe hyperthyroidism in any brain region except the hypothalamus. Further research is thus needed to clarify the mechanisms mediating the numerous biochemical and psychological effects of hyperthyroidism.

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The pituitary-thyroid axis was investigated in nineteen euthyroid patients with severe diabetic ketoacidosis. A 'low T3 syndrome' was found, with the following characteristics: lowered serum concentrations of triiodothyronine (T3), increased reverse triiodothyronine (rT3), slightly low thyroxine (T4), normal thyrotrophin (TSH), slightly increased triiodothyronine uptake (RT3U) values, and a blunted TSH response to thyrotrophin-releasing hormone (TRH). These disturbances in thyroid-function tests required several days good control of the diabetes to be corrected, at least partially. The data suggest the presence of an abnormal extrathyroidal T4 metabolism as well as a pituitary defect. Caution is recommended in the interpretation of thyroid-function tests during and several days after the treatment of diabetic ketoacidosis.

The 24‐h patterns of tissue thyroid hormone concentrations and type II 5′‐ and type III 5‐iodothyronine deiodinase (5′D‐II and 5D‐III, respectively) activities were determined at 4‐h intervals in different brain regions of male euthyroid rats entrained to a regular 12‐h light/12‐h dark cycle (lights on at 6:00 a.m.). Activity of 5′D‐II, which catalyzes the intracellular conversion of thyroxine (T4) to 3,3′,5‐triiodo‐l‐thyronine (T3) in the CNS, and the tissue concentrations of both T4 and T3 exhibited significant daily variations in all brain regions examined. Periodic regression analysis revealed significant circadian rhythms with amplitudes ranging from 9 to 23% (for T3) and from 15 to 40% (for T4 and 5′D‐II) of the daily mean value. 5′D‐II activity showed a marked nocturnal increase (1.3–2.1‐fold vs. daytime basal value), with a maximum at the end of the dark period and a minimum between noon and 4:00 p.m. 5D‐III did not exhibit circadian patterns of variation in any of the brain tissues investigated. Our results disclose circadian rhythms of 5′D‐II activity and thyroid hormone concentrations in discrete brain regions of rats entrained to a regular 12:12‐h light‐dark cycle and reveal that, in the rat CNS, T3 biosynthesis is activated during the dark phase of the photoperiod. For all parameters under investigation, the patterns of variation observed were in part regionally specific, indicating that different regulatory mechanisms may be involved in generating the observed rhythms.