Diurnal metabolic profiles in hyperthyroidism

Abstract. Hormone and metabolite profiles during a 12 h period of normal meals and activity were examined in nine hyperthyroid subjects with Graves' disease and sixteen matched controls. Six hyperthyroid subjects were restudied when euthyroid on carbimazole and thyroxine. Thyrotoxic patients had mild fasting hyperglycaemia (mean pL SEM blood glucose, 5·5 pL 0·2 v. 4·8 pL 0·1 mmol/l, P < 0·01), elevated blood glycerol (0·15 pL 0·02 v. 0·08 pL 0·01 mmol/l, P < 0·001) and elevated plasma non-esterified fatty acid (NEFA) concentrations (0·91 pL 0·06 v. 0·58 pL 0·03 mmol/l, P < 0·001) when compared to controls. Fasting blood concentrations of the gluconeogenic precursors lactate, pyruvate and alanine, blood ketone body concentrations and circulating insulin and growth hormone levels were similar in hyperthyroid and control subjects. Blood glucose responses to meals were exaggerated and the mean 12 h blood glucose was increased (6·1 pL 0·1 v. 5·5 pL 0·1 mmol/l, P < 0·01) in hyperthyroidism. Similarly, hyperlactataemia and hyperpyruvicaemia were observed after meals. Blood ketone body, blood glycerol and plasma NEFA levels showed exaggerated pre-prandial peaks and the mean 12 h values for blood glycerol (0·12 pL 0·01 v. 0·08 pL 0·01 mmol/l, P < 0·01) and plasma NEFA (0·71 pL 0·03 v. 0·53 pL 0·04 mmol/l, P < 0·01) were increased. Concentrations of insulin and growth hormone remained similar to control values throughout the study period. Blocking therapy with carbimazole and thyroid hormone replacement with thyroxine for 5–10 months suppressed blood glycerol, plasma NEFA and blood ketone body levels to normal or subnormal values but had no effect on the elevated blood glucose, blood lactate or blood pyruvate profiles. Graves' disease with hyperthyroidism is thus associated with abnormalities of carbohydrate metabolism which are not restored to normal by 5–10 months oral antithyroid therapy. The changes in lipid metabolism in hyperthyroidism are normalized by this treatment.     

儿童体成分与甲状腺激素关系的研究

对81名的8～12岁男、女学生进行了甲状腺激素的测定，并按体脂百分比分为肥胖组、中等组、消瘦组。肥胖组游离三碘甲状腺原氨酸（FT3）值显著高于其它两组（P＜0.05），中等级高于消瘦组（P＜0.05）。对体成分各指标、游离甲状腺激素（FT4）水平的相关分析显示：体脂肪食量与FT3有正相关关系（P＜0.01）。     

In vivo action of a single injection of thyroxine on the cerebellar protein synthesis and cellular multiplications, in normal and hypothyroid young rats

The effect of a single dose of thyroxine on the cerebellar protein synthesis has been studied in 6, 10 and 14-day-old normal and hypothyroid rats. Doses of 10, 30 and 50 μg thyroxine were studied 24 hours after injection. Furthermore, a dose of 30 μg thyroxine was studied 3, 12, 24, 48 and 72 h post-injection.
Hypothyroidism reduced the cerebellar weight compared to normal animals. A single dose of thyroxine did not change this parameter in the normal and hypothyroid animals. But the cerebellar protein content increased significantly 12 h after thyroxine injection in hypothyroid animals and 48 h later in normal animals.
In hypothyroid rats, the effect of thyroxine on the relative specific radioactivity (RSA) of protein was optimal for a dose of 30 μg thyroxine. This RSA of proteins decreased at 6 days and increased at 10 and 14 days postinjection.
In normal animals the effect of thyroxine on the RSA of proteins was maximal for a dose of 10 μg in 6 and 10–day-old animals only.
In 6–day-old normal, as well as in hypothyroid animals, thyroxine treatment increased RSA of DNA throughout the experimental period, whereas the RSA of DNA increased during the first 72 h of the hormonal treatment in the hypothyroid animals, but only after 48 h in the normal ones.
Thus, the effect of a single dose of thyroxine on both cerebellar protein synthesis and cellular divisions was more rapid and marked in hypothyroid animals than in normal ones. Consequently, the nervous structures of hypothyroid animals were more sensitive to thyroxine than those of normal animals. During the ontogenetic development, thyroid hormones rather seemed to stimulate cell multiplications and its effect on protein synthesis seemed subsequent to cell multiplications.     

Effect of insulin induced hypoglycaemia on thyroid function and thyroxine turnover

Abstract. The effect of long-term hypoglycemia induced by insulin on thyroid metabolism has been investigated in 13 normal subjects. No modification of the uptake or release of radioactive iodine by the thyroid has been observed. A significant increase of circulating thyroxine was found for as long as 8 h after insulin injection. Turnover studies with radioactive thyroxine indicate that during the period of insulin administration, there is a slower disappearance rate of labelled thyroxine from the plasma which occurs simultaneously with a significant drop of the hepatic radioactivity. It seems likely that the enhanced concentration of serum thyroxine is related to the release of thyroxine molecules stored in the liver.     

Thyroid hormone can restore the audiogenic seizure susceptibility of hypothyroid DBA/2J mice

The audiogenic seizure (AS) susceptibility of $\text{DBA}\text{2}\text{J}$ (D2) mice could be suppressed by administration of the antithyroid drug 6-n-propyl-2-thiouracil from 3 days before birth until the time of AS testing (19 days after birth). This treatment effectively induced hypothyroidism. The AS susceptibility of these mice, however, could be almost completely restored by thyroxine replacement from postnatal day 1 through postnatal day 17. The restoration of AS susceptibility by thyroxine replacement was not accompanied by a corresponding restoration of normal serum thyroxine and estimated free thyroxine levels. These observations suggest that thyroid hormone may influence AS susceptibility at some early critical stage of brain development and may be an important requirement for the development of AS susceptibility in D2 mice.     

Update on Thyroid Diseases

A discussion of the regulation of thyroid function, the synthesis, release, and biologic effects of the thyroid hormones is presented as the basis for understanding and appreciating the array of thyroid diseases, their classification, diagnosis, and management.     

A case of familial thyroxine binding globulin excess associated with growth hormone deficiency

A 7 years 3 months old Japanese boy with familial thyroxine binding globulin (TBG) excess associated with growth hormone (GH) deficiency is reported. The patients height was 106.4 cm (- 2.86 s.d.) and his bone age was 5 years and 3 months. He had no goiter and his developmental milestones were normal. The serum thyroid stimulating hormone (TSH) was 2.8 μU/mL, triiodothyronine (T₃) 3.1 ng/mL, thyroxine (T₄) 23.4 μg/dL and free T₄ 1.8 ng/dL. The serum TBG level was beyond 80.0 μg/mL, with normal TSH response to the thyrotropin-releasing hormone (TRH) test. Familial study revealed that his grandmother, mother, uncle, younger sister and younger brother had high TBG and T₃ levels, thus an X-linked co-dominant transmission was suggested. The peak GH responses to insulin and clonidine hydrochloride were 5.8 and 8.2 ng/mL, respectively. The mean nocturnal GH concentration was 2.5 ng/mL. His growth velocity increased from 4.8 to 8.4 cm/year and his serum TBG levels decreased gradually after human growth hormone (hGH) treatment.