Low Iodine Diet Research Articles

Hypothyroidism increases pancreatic thyrotropin-releasing hormone concentrations in adult rats.

The effect of hypothyroidism on pancreatic TRH (P-TRH) and P-TRH-degrading activity (P-TRH-DA) was studied in adult rats. Hypothyroidism was induced in three groups during 4, 6, or 9 weeks by propylthiouracil (PTU) in drinking water and a low iodine diet (LID). Another group received PTU-LID for 6 weeks, followed by 5 weeks on a normal diet to restore euthyroidism. A possible toxic effect of PTU per se was eliminated by treating one control group with PTU and T3. P-TRH and TRH-DA were measured by specific RIA. In the hypothyroid groups, P-TRH concentrations (mean +/- SEM) were increased 10-fold (6.95 +/- 2.09; 5.51 +/- 1.3; 9.79 +/- 3.3 pg/(mg X 100 g BW), respectively, with a control value of 0.55 +/- 0.39, P less than 0.01). This increase was reversible, as shown by the group on PTU-LID followed by a normal diet (0.58 +/- 0.39, NS). P-TRH-DA present in the control group was decreased after 4 weeks of PTU-LID treatment and totally abolished after 6 and 9 weeks of PTU-LID treatment. In conclusion, these results suggest that thyroid status modulates P-TRH concentrations. This effect may be due to the disappearance of the TRH-DA in response to hypothyroidism. P-TRH stores may be regulated by the enzyme(s) involved in P-TRH-DA.

Precocity of the endothelial proliferation during a course of rapid goitrogenesis.

Thyroid hyperplasia was induced in C3H mice by a low iodine diet feeding supplemented with propylthiouracil. The morphological modifications associated to the development of hyperplasia were analyzed at light microscopical level and the cellular proliferation was studied by autoradiography after a pulse labelling with [3H]thymidine. The initial modification during the course of hyperplasia is the development of the vascularization. It includes the dilatation of the capillaries, which occurs before any extended modification of the follicular cells and any change of the thyroid weight, and the proliferation of endothelial cells which starts earlier than that of follicular cells.

Dedifferentiation of a transplantable papillary thyroid carcinoma over a 15-year period.

Fischer 344 rats on a prolonged low-iodine diet developed thyroid nodules which were transplanted subcutaneously into 33 thyroidectomized rats. One graft took and gave a papillary carcinoma. Serially transplanted syngeneically at 3- to 4-month intervals, it became autonomous in third generation hosts. With electron microscopy examination it was microfollicular in year 8 and anaplastic, with totally unpolarized epithelial cells, in year 15. Basement membrane present in year 1 was no longer visible in specimens of years 8 and 15. Tight and gap junctions still present in year 8 were absent in year 15, although a few desmosomes persisted. From years 8 to 15, free ribosomes and microfilaments became more frequent, whereas the number of mitochondria and the development of the Golgi complex declined.

Capillary endothelial cell multiplication in adipose tissue pads on the thyroid during the feeding of thiouracil.

It has been reported that blood capillaries in adipose tissue pads on the upper and lower poles of the thyroid gland enlarge when Fischer rats are fed thiouracil (TU) in a low iodine diet. To test whether the enlargement is accompanied by proliferation of the endothelial cells, [3H]thymidine was injected into rats fed the TU-containing diet, and labeling of the endothelial cells was studied by autoradiography. Nuclear labeling of the capillary endothelial cells was observed in the mixed brown and white adipose tissue (BAT and WAT, respectively) pads on the thyroid. After a single pulse of [3H]thymidine, 10% of the nuclei were labeled at 10 days (the peak labeling), and labeling decreased thereafter. To test whether the adipose tissue was stimulated because of the poor nutritional quality of the low iodine diet, Purina Laboratory Chow (a nutritionally adequate diet) was tested and produced the same result. To test whether TU had a direct effect, 5 micrograms T4/100 g BW were given daily; there was then no response to the TU, suggesting that the effect was due to an elevated circulating concentration of TSH. The effect was generally restricted to the adipose tissue pads on the thyroid. There was no response in interscapular BAT, epididymal WAT, or sc WAT. However, there was a response in small clusters of adipocytes embedded in inguinal sc WAT. The results are consistent with the idea that the effects are directly or indirectly due to elevated circulating TSH levels.

Effects of KClO4 in propylthiouracil-hypothyroid rats.

In this study we investigated further the antigoitrogenic effect of ClO4 in rats on a low iodine diet (LID) and 6-propyl-2-thiouracil (PTU). The thyroid weight of rats on the mixed goitrogen was initially similar to that of animals on PTU, decreasing to values obtained in rats treated with ClO4 alone by 10 days. Despite the differences in thyroid weight, rats treated during an identical period with PTU or mixed goitrogen develop hypothyroidism to a comparable degree as far as can be assessed by the thyroidal 127I content, plasma T4, T3 and TSH concentrations, and pituitary TSH content. Moreover, it was observed that there were differences in plasma insulin and glucose levels in these hypothyroid animals. The plasma insulin and glucose levels of rats on PTU are comparable to those found in control rats. In rats on mixed goitrogen, both plasma insulin and glucose levels are initially maintained within the normal ranges, and then decline over the subsequent days of treatment. Within the treatment period studied here, plasma insulin and glucose levels were higher for rats on PTU than for animals on ClO4, PTU + ClO4, or thyroidectomized (Th) animals. We have obtained further evidence of the hypothyroid state of rats on these goitrogen regimens based on measurements of pituitary and plasma GH levels and liver mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD). The PTU-treatment decreased the liver alpha-GPD activity to a comparable degree to that of mixed goitrogen. Moreover, both PTU + ClO4 and PTU-treatment resulted in a state of hypothyroidism intense enough to induce effects on growth, and plasma and pituitary GH levels comparable to that of Th animals. However, the values for rats on mixed goitrogen appear to be below the PTU data. The present findings appear to be consistent with the view that TSH is not the unique factor determining the size of the resulting goitre. The results are discussed in relation to the hypothesis that: 1) the antigoitrogenic effect of ClO4 could be associated with changes in the ability of the thyroid tissue to bind TSH, or with a step beyond TSH binding, and 2) the different endocrine and metabolic states of rats on PTU or PTU + ClO4, shown by their different plasma insulin, GH and glucose levels, may play an important role in determining the thyroid weight response to TSH.

The effect of thyrotropin (TSH) levels on follicular cluster formation from grafted monodispersed rat thyroid cells.

The effect of experimental conditions which alter TSH levels on the number and size of the multifollicular thyroid clusters which develop from inoculated monodispersed thyroid cells was explored. Five week-old male Fischer rats were used as thyroid cell donors and recipients. The recipients were totally thyroidectomized (Tx) 1 week before thyroid cell transplantation (group A), hemithyroidectomized (hemi Tx) 1 week before transplantation (group B), or Tx 1 day before grafting (group C). Additional groups of recipients included intact animals maintained on low-iodine diet (LID) (group D), and on normal diet (ND) (group E). The FD50, the number of grafted cells required to produce at least one follicular cluster in 50% of the transplant sites, was the lowest in group A and the highest in group E. The TSH levels in the serum on the day of cell inoculation were highest in group A and lowest in group E. Large follicular clusters tended to be more frequent in groups A and C than in group B, but the data were variable; no large clusters were found in groups D or E. The TSH levels in groups A and C 28 days after cell implantation were higher than in group B. The FD50 is thus dependent on the concentration of circulating TSH for initiation of follicle formation; large follicular clusters result from continued elevation of TSH levels.

Morphological and functional changes during thyroid hyperplasia and involution in C3H Mice: evidence for folliculoneogenesis during involution.

Involution of thyroid hyperplasia was induced in C3H mice by discontinuing a goitrogenic treatment (low iodine diet supplemented with 0.25% propylthiouracil) and refeeding a normal iodine diet. Thyroid involution was studied by morphological, histochemical, autoradiographic, and stereological methods. The onset of the involution was characterized by an early accumulation of colloid, the presence of necrotic cells in the follicular lumina, and the appearance of homogeneous microcavities in the epithelial layers. The intraepithelial microcavities had the same morphological and functional properties as the follicular lumina. They were limited by a membrane covered with microvilli; polysaccharides and peroxidase activity were detected on their membranes, and 125I-labeling was marked in their lumina. Thin serial sections demonstrated that the microlumens originated from the intercellular space; plasma membranes differentiated into junctional complexes, and a narrow lumen limited by a membrane covered with short microvilli was formed in the intercellular space between the junctions. Later on, the newly formed microlumens fused to form new follicles with a cloverleaf pattern. As a consequence of the folliculogenesis, the total number of follicles doubled after 8 days of involution. This increase in number was mainly due to the presence of a population of small follicles. The folliculogenesis was associated in the first 4 days of involution with an active cellular multiplication which compensated for the early cell necrosis and led to a doubled number of epithelial cells. The increase in the total number of follicles and cells could partially explain the persistence of a relatively high thyroid weight after involution of hyperplasia.

Low iodine diet in I-131 ablation of thyroid remnants.

A low-iodine diet was developed for used in decreasing iodine intake and excretion in patients undergoing evaluation with radioactive I-131 for ablation of thyroid remnants as treatment for thyroid cancer. It has been demonstrated to effectively lower iodine excretion to less than 25% of basal values. Preliminary calculations suggest that such iodine depletion may be potentially useful in increasing the radiation dose per mCi of administered activity in I-131 ablative therapy.

Lack of refractoriness to stimulation with long acting thyroid stimulator of thyroid hormone synthesis and thyroid hormone secretion in mice in vivo.

The present study was undertaken to examine whether long acting thyroid stimulator (LATS) induces refractoriness of thyroid hormone synthesis and thyroid hormone secretion to the stimulator in vivo. Male DDY mice fed with a low iodine diet and given 5 micrograms/ml of triiodothyronine (T3) in drinking water and libitum for 4 days were injected with 0.025 ml of LATS positive serum (1000%/0.25 ml in rhe McKenzie bioassay) ip every 24 h for 9 days. Groups of 5 mice were sacrificed before and 1, 3, 5, 7 and 9 days after the first injection of LATS for the determinations of serum thyroxine (T4) concentrations, the 1 h thyroid 131I uptake and thyroid weight. Control mice were injected with LATS negative pooled normal sera. Serum T4 concentrations elevated significantly 24 h after the 3rd injection of LATS and remained elevated until the end of the experiment. One hour thyroid 131I uptake elevated about 3-fold 24 h after the first injection of LATS. It further increased 24 h after the 3rd injection of LATS to 10-fold of the value for control animals and stayed elevated at this same level for the remainder of the study. These results indicate that stimulating effects of LATS on thyroid hormone synthesis assessed by thyroid 131I uptake and thyroid hormone secretion assessed by serum T4 concentrations were not diminished by the prior administration of the stimulator. These findings suggest that LATS does not induce refractoriness of either thyroid hormone synthesis or thy roid hormone secretion to the stimulator in mide in vivo.

Lipolysis and blood capillary enlargement in adipose tissue pads on thyroids of rats fed thiouracil.

In the young adult male Fischer rat there are mixed brown and white adipose tissue pads on the surface of the thyroid gland at the upper and lower poles of the lobes. When the thyroid gland was stimulated by feeding the rats 0.25% thiouracil in a low iodine diet, these adipose tissue pads became much less prominent. Examination of histological sections revealed that there were marked morphological changes in these pads. After feeding the animals the thiouracil-containing diet, thyroids and the adipose pads were fixed by perfusion with a solution of 2% formaldehyde, 2.5% glutaraldehyde, and 3% dextran in cacodylate buffer and postfixed in 1% osmium tetroxide in buffer, and whole lobes were embedded in Epon. The lobes were sectioned serially starting at one pole, and sections were usually examined every 0.3 mm. Adipose tissue was found only within 1.5 mm from each pole. Although thyroid tissue showed changes within 1 or 2 days, no obvious morphological changes were seen in the adipose tissue pads until appr...

Acute effects of iodine on the stimulated rat thyroid.

Rats fed a low iodine diet (LID) for 5 weeks were given 125I as NaI to prelabel their thyroids; 24 h later, they were injected ip with 1 mg KI. They were then killed at different time intervals of up to 4 h. Thyroids of control animals not injected with KI were hyperplastic, the tissue showed microfollicles devoid of colloid, thyroglobulin was poorly iodinated, and thyroid peroxidase activity was increased. Within 4 h after KI injections, there was 1) a decrease in thyroid weight, 2) expansion of the follicular lumens of the hyperplastic in thyroid tissue and accumulation of colloid, 3) an increase in the thyroglobulin iodine concentration, and 4) a decrease in the thyroid peroxidase activity. Some of these changes started to occur as early as 60 min after KI administration. By that time, using the microprobe, most of the organically bound iodine was detectable inside the follicular cells. Radioiodine (125I) used to prelabel the thyroids was accumulated inside the follicles during the entire observation period. The serum TSH level was elevated and did not decrease after KI administration. It is concluded that excess iodine in LID rats may produce acute morphological and biochemical changes which seem to be a direct effect of iodine not mediated by modifications of TSH. The distribution of organically bound iodine, as determined by the microprobe, and the biochemical studies were interpreted as suggesting intracellular thyroglobulin iodination in these stimulated rat thyroids.

Antithyroid effect of 2,3-dihydroxypyridine in vivo and in vitro.

AbstractThe antithyroid effect of 2,3-dihydroxypyridine (2,3-DHP) was investigated in vivo and in vitro. Thyroid studies were carried out on two groups of rats; one group of 14 rats were fed a low-iodine diet containing 1% 2,3-DHP for 25 days, and a control group of 12 rats received low-iodine diet alone. 2,3-DHP-treated rats had reduced thyroid function with a significant rise in serum thyrotropin (TSH) levels and decreased serum triiodothyronine (T3) levels; thyroxine (T4) and T3 contents of the thyroid gland were 20 and 10%, respectively, lower than those of controls. In vitro, 2,3-DHP inhibited peroxidase activity, and its antiperoxidase potency was similar to the commonly used thioureylene antithyroid drug, propylthiouracil. In addition, 2,3-DHP was a much weaker inhibitor of the thyroid conversion of T4 to T3 in vitro than propylthiouracil. 2,3-DHP represents a new class of antithyroid drug and its main action appears to be inhibition of peroxidase-catalyzed thyroid hormone formation in the thyroid ...

Are iodine-deficient rats euthyroid?

Inhabitants of many severe endemic goiter areas have low serum T4 and high circulating TSH, despite normal levels of T3. This situation may be produced experimentally chronically feeding rats a low iodine diet (LID). We fed rats a Remington-type LID and gave them 1% NaClO4 in their drinking water for 2 days. After this, the animals were divided into three groups. One group was fed LID, supplemented with 5 micrograms I/rat.day and was used as the control group. Another group was fed LID alone. The third group was fed LID and given 1% NaClO4 to drink. The latter treatment was used to induce severe hypothyroidism. Animals were killed 1, 2, 3, and 5 weeks after the onset of these treatment schedules. The following measurements were made on some or all groups of animals: body and thyroid weights; thyroidal I content; soluble labeled iodoprotein profile; thyroidal labeled iodoamino acid distribution pattern; plasma T4, T3, and TSH; pituitary GH content; and liver intramitochondrial alpha-glycerophosphate dehydrogenase and cytosolic malic enzyme activities. T4 and T3 concentrations were also measured in liver nuclei of the animals killed 5 weeks after the onset of treatment. As assessed from various indices of thyroid function, the LID rats became iodine deficient, although not as markedly as those given LID and ClO4-, The plasma T4 decreased to undetectable levels, and plasma TSH increased, whereas circulating T3 remained normal throughout in the LID rats. In rats given LID and ClO4-, plasma T4 decreased sooner than in rats given LID alone; plasma T3 levels also became undetectable, and TSH increased more markedly and sooner than in rats given LID alone. As measured at the end of 5 weeks of treatment, pituitary GH content, and liver alpha-glycerophosphate dehydrogenase and malic enzyme activities were lower in rats given LID than in the euthyroid LID- and I--treated controls. They were not, however, as markedly reduced as in the severely hypothyroid LID- and ClO4--treated rats. In spite of normal plasma T3 levels, the concentration of T3 in liver nuclei of the rats given LID alone was significantly lower than that of the LID- and I--treated controls. The results show that the thyrotrophs, somatotrophs, and livers of rats given LID alone are not like those of euthyroid rats despite normal circulating T3 levels. In iodine-deficient rats, there is a discrepancy between the measured indices of thyroid hormone action in the liver and the circulating T3 level, but not between biological activity and liver nuclear T3 concentration. It remains to be seen whether the same is true in the anterior pituitary.

Effect of chronic iodide supplements on thyroid secretion: the role of lysosomes.

The role of thyroid lysosomes in hormonal secretion has been studied in rats fed a low iodine diet and receiving chronic increasing iodide supplements. Thyroid secretion was assessed by plasma TSH, T3, and T4 levels and by the concentration and degree of iodination of thyroglobulin (Tgb). Lysosomal activity was evaluated by the total activity of four lysosomal acid hydrolases and by the integrity and fragility of the lysosomal membrane, which were assessed by the latency of acid phosphatase activity and the susceptibility of the particles to physicochemical manipulations. In glands from animals on a low iodine intake and under chronic TSH hyperstimulation, the integrity of the lysosomes was modified (increased free, but sedimentable, acid phosphatase activity), and the lysosomal membrane cohesion was high (increased resistance to freezingthawing and acid autolysis). In animals receiving increasing physiological iodide supplements, plasma TSH levels were normal, and the size of the intrathyroidal iodine pool autoregulated thyroid secretion; in spite of the increased concentration and iodine content of Tgb, the plasma levels of T3 and T4 remained fairly constant. The total activities of the four lysosomal enzymes tested increased gradually with the iodide supply. The integrity and stability of the lysosomes were not modified. Iodine at high pharmacological doses was not a lysosome stabilizer but induced a labilization of the lysosomal membrane. We suggest that lysosomes may participate in the autoregulation of thyroid secretion by the intrathyroidal iodine pool; the synthesis of new lysosomal hydrolases is induced, which may gradually be involved in the degradation of cellular constituents rather than in the hydrolysis of extracellular Tgb.

Correlated functional and morphometric study of thyroid hyperplasia induced by iodine deficiency.

The effect of feeding a low iodine diet (LID) on the thyroids of mice of both sexes for 1–8 weeks was investigated. Morphometric, autoradiographic, and chemical methods were used. Morphologically, the thyroid response to LID could be divided into two successive phases. During the first 4 weeks, the glandular weight remained constant, but changes in the relative volumes of various tissue components occurred, i.e. an increase of the blood vessels and the follicular epithelium, contrasting with a decrease of the colloid. The epithelial height almost doubled. [3H]Thymidine incorporation indexes (TII) increased by the first week in endothelial cells, earlier than in the follicular cells. At all times studied, more than 40% of the TII was related to nonfollicular cells. During the second period (5–8 weeks), the glandular weight increased, but the relative volumes of all of the tissue components, the epithelial height, and the TII were almost stabilized; all of the glandular components grew at a similar rate. Fu...

Site of Iodination in Hyperplastic Thyroid Glands Deduced from Autoradiographs*

We have tried to ascertain the site of iodination in the chronically stimulated, hyperplastic thyroid gland of rats. Rats were fed propylthiouracil in a commercial rat diet for 10 days. Then the diet was changed to a low iodine diet for 5 days. To label the gland, 10 mCi of 125I-iodide was injected into the left heart ventricle. Ten seconds later the animal was perfused through the left ventricle with a fixative solution containing a goitrogen to block further iodination, and stable iodide to help extract uncombined radioiodide. Electron microscopic autoradiographs prepared from the fixed thyroids show strong labeling over the lumen of the follicle and no consistent labeling of any other site or organelle. We conclude that the site of iodination in the chronically stimulated, hyperplastic thyroid is the follicular lumen, i.e. the same as that in the normal gland.

Maternal thyroid function is the major determinant of amniotic fluid 3,3',5'-triiodothyronine in the rat.

3,3',5'-triiodothyronine, (rT(3)), is easily measured in human amniotic fluid (AF) during the second and third trimesters. To determine if AF rT(3) levels are maintained by either maternal or fetal thyroid function, or both, models of fetal hypothyroidism (FH), maternal hypothyroidism (MH), and combined maternal and fetal hypothyroidism (MFH) were developed in pregnant rats. Hormone analyses of maternal and fetal serum and AF were performed at term. Thyroxine (T(4)) and 3,3',5-triiodothyronine (T(3)) were not detectable in the sera and AF of term fetuses in all groups. MFH rats were prepared by administration of methimazole to the dams, and in some experiments, by maternal thyroidectomy and a low iodine diet as well. In the MFH groups from the three experiments serum thyrotropin (TSH) was markedly elevated in the dams and in the fetuses. FH rats were prepared by administering T(4) by various routes to dams treated according to the MFH protocols and serum TSH was elevated in fetal serum. Analysis of FH maternal serum T(4), T(3), and TSH concentrations suggested mild maternal hyperthyroidism or hypothyroidism depending upon the schedule of T(4) administration. The MH groups were prepared by maternal thyroidectomy and in all experiments the fetuses had normal serum TSH concentrations. The degree of maternal hypothyroidism in the MH and MFH groups was equivalent. The mean concentration of AF rT(3) in normal rats in three experiments was 28.4+/-2.5 ng/dl (+/-SEM). In the three experiments, AF rT(3) was undetectable or markedly reduced in the MH and MFH rats and was normal in the FH rats. These results in the amniotic fluid could not be explained by transfer of rT(3) from fetal serum to the AF because fetal serum rT(3) concentrations in these various models did not correlate with AF rT(3) concentration. Furthermore, infusion of large doses of rT(3) in MFH dams resulted in a 35-fold elevation in maternal serum rT(3) concentration, a twofold elevation in fetal serum rT(3) concentration, and only a minimal increase in AF rT(3). These studies demonstrated that, in the rat, the maternal thyroid has the dominant role in maintaining AF rT(3), whereas little effect of fetal thyroid status on AF rT(3) could be demonstrated. Transfer of maternal rT(3) or of fetal rT(3) derived from maternal T(4) to the AF do not appear to be the mechanisms whereby the maternal thyroid maintains AF rT(3).

Alterations in thyrotropin (TSH) binding in iodine-deficient rats

Thyrotropin (TSH) is thought to stimulate thyroid activity and growth by binding to TSH receptors on thyroid plasma membranes. Iodine depletion has been shown to increase the sensitivity of the thyroid to the goitrogenic effects of TSH. The present investigation was performed to determine if chronic iodine depletion altered either the number or the affinity of TSH receptor sites in the thyroid. Six paired experiments were performed comparing the binding of 125I-labeled bovine TSH to a particulate fraction of thyroid from male Sprague-Dawley rats that had received regular (C) or low iodine diet (LID) for 3 to 7 months. The number of TSH receptors and the association constants of these receptors were calculated from Scatchard plots and binding was compared with glandular concentrations of DNA, RNA, protein, plasma membrane markers (5′-nucleotidase, Mg 2+ ATPase, Na +, K + ATPase), and per thyroid gland. (1) The weights of all animals were initially similar but after 3 to 7 months the LID group (638 ± 139 g (mean ± 1 SD)) was heavier than the C group (544 ± 45 g ( P < .01)). (2) Serum TSH concentrations in the LID group (5231 ± 547 ng/ml) were higher than those in the C group (850 ± 221 ng/ml) ( P < .005). (3) Thyroid weight, thyroid weight per animal weight, DNA, RNA, total protein, Mg 2+ ATPase, Na +, K + ATPase, and 5′-nucleotidase were all increased in the LID group ( P < .005). Histological examination demonstrated that the thyroid enlargement was primarily due to an increase in number of follicle cells, or hyperplasia. (4) The concentration of TSH receptors (maximum binding capacity) per DNA content was similar in the C and LID groups. (5) The concentration of TSH receptors per plasma membrane marker decreased in the LID group ( P < .01) primarily because of the large increase in amount of plasma membrane. (6) The total number of TSH receptors per thyroid gland or TSH receptor content increased from 0.52 ± 0.16 × 10 14 in the C group to 2.27 ± 0.79 × 10 14 in the iodine-deficient animals ( P < .001), and the association constant in these animals (1.28 ± .27 × 10 8 M −1) was also higher than that in the C group (0.68 ± 0.16 × 10 8 M −1) ( P < .001). Thus, chronically iodine-deficient rats developed increased serum TSH concentrations and enlarged hyperplastic thyroid glands. Although the number of TSH receptors per DNA or cell did not change in the respective groups, the TSH receptor content and the association constant of these receptors for TSH in the thyroid gland of the iodine-deficient animals increased. It therefore appears that increased serum TSH concentrations in iodine-deficient rats exerts a positive regulatory effect on its own receptors and that alterations in serum TSH level modulate the TSH receptor. Whether this effect is due to a direct effect of TSH on the TSH receptor or an indirect effect secondary to thyroid growth is unknown.

Does-related effect of growth hormone on thyroidal radioiodine uptake.

Even though growth hormone was reported to play a role in mammalian calorigenesis, few studies have examined its effect on thyroid function. Consequently, the modulatory effect of bovine growth hormone (BGH) on thyroid incorporation of 131I was studied in hypophysectomized (H) rats. Not surprisingly, H recipients fed a low iodine diet consistently displayed greater thyroidal uptakes of radioactive iodine than recipients given regular diets. Furthermore, thyroid radioactive counts increased predictably in direct proportion to the quantity of bovine thyrotropin administered. Larger doses of BGH suppressed the thyroidal uptake of 131I whereas smaller doses either had no effect or enhanced thyroidal activity. Thus, these results affirm that radiolabelled and non-radiolabelled iodine compete in thyroid metabolic processes and furthermore demonstrate that high doses of BGH inhibit thyroid activity.

Iodine Deficiency and Brain Development in the Rat

An assessment was made of the influence of low-iodine diet on somatic and brain development at birth (day 0) and 21 days postnatally in the rat. The rat mothers were proven to be iodine-deficient by assay of plasma thyroxine and thyroid stimulating hormone prior to mating, an at 21 days postnatally, when maternal thyroids were removed, weighed and stored for subsequent iodine analysis, along with those of the offspring. There were no significant differences in body weight or brain weight of the offspring at birth, or in the content of DNA or protein. However, at 21 days there was a significant reduction in body weight (21.7%) and whole brain weight (7.9%, P less than 0.2) which was associated with a significant fall n cholesterol content (12.4%, P less than 0.05) and protein level (9.6 %, P less than 0.01), while DNA was not significantly affected (6%). The greatest reduction in weight was seen in the cerebellum. The thyroids in these rats were double normal size, showed follicular cell hypertrophy and absence of colloid histologically, and contained 8% of the iodine content of controls. It is concluded that iodine deficiency retards both somatic and brain development, the change in the latter case being expressed as a reduction in cell size in the cerebral hemispheres and cerebellum, along with reduced myelination throughout the brain.