Thyroidal 131I Uptake Research Articles

Patterns of TSH response to TRH in children with hypopituitarism

The TSH response to TRH was studied in 42 children with hypopituitarism. Basal TSH was similar to the control group except in seven patients who had elevated values (Group A). These children also had an altered TSH response to TRH but normal increments in T4, T3, and 131I thyroid uptake after administration of bTSH. Three different patterns of TSH responses to TRH were observed in patients with normal basal TSH: delayed and exaggerated response (Group B, n=15), deficient response (Group C, n=4), and normal response (Group D, n=16). Some patients of groups A, B, and C with blunted basal growth velocity had an improved growth rate with T4 therapy. However, a better response was observed when hGH and T4 were administered simultaneously. The following conclusions were drawn: (1) high immunoreactive TSH in the presence of a thyroid gland responding normally to TSH suggests a dissociation between the biologic and immunologic activity of serum TSH; (2) an exaggerated and delayed response to TRH was frequently found in secondary hypothyroidism and suggests hypothalamic TRH deficiency; (3) an impaired TSH response to TRH is less frequent and suggests a pituitary abnormality; (4) patients with a normal response to TRH probably have normal hypothalamic-pituitary thyroid axis. The TRH test is useful in the diagnosis of hypothalamic-pituitary thyroid abnormalities and helps to unmask thyroid dysfunction. A number of such patients with stunted growth benefit from thyroid therapy. The TSH response to TRH was studied in 42 children with hypopituitarism. Basal TSH was similar to the control group except in seven patients who had elevated values (Group A). These children also had an altered TSH response to TRH but normal increments in T4, T3, and 131I thyroid uptake after administration of bTSH. Three different patterns of TSH responses to TRH were observed in patients with normal basal TSH: delayed and exaggerated response (Group B, n=15), deficient response (Group C, n=4), and normal response (Group D, n=16). Some patients of groups A, B, and C with blunted basal growth velocity had an improved growth rate with T4 therapy. However, a better response was observed when hGH and T4 were administered simultaneously. The following conclusions were drawn: (1) high immunoreactive TSH in the presence of a thyroid gland responding normally to TSH suggests a dissociation between the biologic and immunologic activity of serum TSH; (2) an exaggerated and delayed response to TRH was frequently found in secondary hypothyroidism and suggests hypothalamic TRH deficiency; (3) an impaired TSH response to TRH is less frequent and suggests a pituitary abnormality; (4) patients with a normal response to TRH probably have normal hypothalamic-pituitary thyroid axis. The TRH test is useful in the diagnosis of hypothalamic-pituitary thyroid abnormalities and helps to unmask thyroid dysfunction. A number of such patients with stunted growth benefit from thyroid therapy.

Hydrochlorothiazide-induced 131I excretion facilitated by salt and water.

Salt intake is restricted under clinical conditions for which thiazide diuretics are customarily used. Dietary iodide intake offsets any effect of thiazide on iodide loss. However, our correlation coefficients relating Na+ to Cl- to I- excretion indicate that as thiazide administration or sodium chloride intake increases renal Na+ and Cl- excretion, I- reabsorption by the nephron coordinately decreases. Increased sodium chloride and water intake by the dog doubled I-excretion rates. Hydrochlorothiazide increased the sodium chloride and water enhanced I-excretion rate as much as eight-fold. Without added NaCl, hydrochlorothiazide increased the excretion rate of 131I by three- to eightfold, acutely. Within five to seven days after 131I oral administration, hydrochlorothiazide (1 or 2 mg/kg twice daily) doubled the rate of 131I disappearance from plasma, reduced the fecal output of 131I, and increased its rate of renal excretion. When hydrochlorothiazide was administered, as much 131I was excreted in the first 24 hours as occurred in 48 hours when sodium chloride and water were given without hydrochlorothiazide. Thiazide administration in customary clinical dosage twice a day with substantial sodium chloride and water for the first two days after exposure to 131I, should therefore facilitate the safe excretion of 131I. This accelerated removal of 131I might be enhanced even more if thyroid uptake of 131I is blocked by administration of potassium iodide, as judged by the greater 131I recovery from thyroidectomized dogs.

Effect of Polybrominated Biphenyls (PBB) on the Pituitary-Thyroid Axis of the Rat

AbstractThe effects of polybrominated biphenyls (PBB) on the pituitary-thyroid axis were investigated in male rats. PBB was administered by gavage for 20 days at 1, 3, or 6 mg/kg/day; controls were gavaged with vehicle alone. PBB treatment had no effect on body weight. There was a definite time- and dose-dependent reduction in plasma thyroxine (T4) levels after 10 and 20 days of PBB administration. Reduced plasma T4 levels were correlated with increased plasma TSH levels at 20 days. In rats treated with 6 mg/kg PBB, an increase in 5-hr thyroidal 131I uptake was seen, with a decrease in 131I incorporation into monoiodotyrosine and an increase in intrathyroidal iodine. In contrast to propylthiouracil, acute administration of PBB had little effect on intrathyroidal radioiodine accumulation and incorporation into iodoamino acids. Liver and thyroid weights remained elevated at 2 and 5 months after the last 1 and 3 mg/kg PBB administration, respectively, and plasma T4 levels were significantly lower than contro...

Effect of 2-mercaptopropionylglycine (MPG) on thyroid function in sub-lethally irradiated mice.

External irradiation resulted in an increase in thyroid131I uptake and plasma PB131I conversion ratio, whereas pretreatment with MPG reduced both the values significantly. Metabolic inhibition is suggested as a possible mechanism of action by the drug.

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.

Alteration of thyroid function in the early stage of subacute thyroiditis.

Measurement of serum triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyroxine-binding-globulin (TGB), antithyroglobulin antibodies (anti-hTg), thyroid 131I uptake and scanning was performed on 12 patients during the early phase of subacute thyroiditis. Serum thyrotropin (TSH) was measured during baseline conditions and following administration of synthetic thyrotropin-releasing-hormone (TRH). The stimulation with exogenous TSH was performed on 7 subjects. 131I uptake was depressed in all patients including those with solitary nodules. Free and total hormone concentrations were elevated in the three cases with diffuse gland involvement, whereas an increase of T3 alone was present in 3 patients with unilobar involvement. In the latter group and in the 2 patients with a nodular form T4, FT3 and FT4 levels were within normal limits. Interruption of the pituitary-thyroid feed-back mechanism with absence of thyrotropin response to TRH occurred in 11 patients, independent of whether thyroid hormone concentrations were elevated or normal. In one patient only with unilateral involvement, TSH responsiveness to TRH was normal while 131I uptake was not raised by exogenous TSH, indicating diffuse cellular damage. The normal values of FT3 and FT4 found in patients with normal T3 and T4 levels seem to exclude the possibility that the free hormones are responsible for the interrupted feed-back which represents the main cause of suppressed iodine uptake. However, it is possible that the pituitary-thyroid axis is responding to transient or light increases of free and total T3 and T4 still within their 'normal range'.

Restricted food intake and annual thyroid cycle of spotted munia

The spotted munia shows a seasonal cyclicity in total daily food intake as well as in thyroid function. The seasonal decline in thyroid activity is preceded by a 50% reduction in food intake. In January, artificially restricting the food consumption to late summer/fall level (by about 50%; 2.5 g/bird/day over 4 days) led to a significant decrease in conversion of monoiodotyrosine (MIT) to diiodotyrosine (DIT), relative proportions of thyroxine (%T 4) and triiodothyronine (%T 3) in the gland, and plasma protein-bound iodine after the injection of a tracer dose of I at almost all points studied. The plasma radioiodohormone fraction (%T x ), as measured by Sephadex gel filtration, was also significantly less than that in the adlibitum-fed controls at all the points studied. These results were confirmed later (May) by direct measurement (radioimmunoassay) of hormone levels when plasma concentration of total and free T 4 and T 3 were found significantly low in similarly treated birds as compared to controls. A 30% restriction in diet (simulating late spring food intake) did not alter percentage thyroidal 131I uptake, MIT/DIT ratio, glandular %T 4 plasma PBI, and %T x but decreased %T 3 in the gland. A constant fixed restricted diet (2.5 g/bird!day, ambient conditions) over 8 months suppressed the seasonal variation in some thyroid activity parameters (% 131I uptake, % thyroidal T 4 and T 3). The declining ambient temperature failed to restore the thyroid of underfed birds to normal winter efficiency. It is concluded that the seasonal lowering of thyroid activity in spotted munia may be partly due to minimal levels of food intake reached in late summer and fall. The increase in thyroid activity in winter may partly result from an increased food intake in response to the low ambient temperature.

Clinical and pathological significance of sibling Graves' disease.

The clinical picture and serum antithyroid antibodies in 16 pairs of siblings with Graves' disease were compared with an age and sex matched group of 32 patients with Graves' disease who did not have a family history of any thyroid disease (control patients). There was a significant difference in frequency and mean titres of antibodies to thyroglobulin between sibling patients. (positive 76.0%) and control patients (positive 40.0 %), but not in microsomal antibodies (sibling; positive 92.0%, control; 92.0%). There were no significant differences in the mean values of 24 h 131I-thyroidal uptake, serum T3U, serum T4 and T3 concentrations before treatment between the two groups. Lymphoid follicles and degeneration of the epithelia were more often found in the thyroid glands of sibling patients than in those of the control patients, when 32 (16 sibling, 16 control) thyroid glands from the same groups in the clinical study, including antibody series, were examined pathologically after subtotal thyroidectomy for Graves' disease. Moreover, there was a strong tendency to increased lymphocyte and plasma cell infiltration in the thyroid glands of sibling patients with Grave's disease. The findings might indicate that Graves' disease is closely related to Hashimoto's thyroiditis, especially in sibling patients with Graves' disease.

Thyroid activity and TSH potency of the pituitary gland and blood serum in response to Cythion and Hexadrin treatment in the freshwater catfish, Heteropneustes fossilis (Bloch)

Effects of Cythion (organophosphorus compound) and Hexadrin (organochlorine compound) on thyroidal activity and thyrotrophic potency of the pituitary gland and blood serum were studied in Heteropneustes fossilis. Reduced thyroid activity as judged by thyroidal 131I uptake and CR (conversion ratio of PB 131I in blood serum in relation to total serum 131I uptake) was noticed within 4 weeks of Cythion and Hexadrin treatment at safe concentration (SC) and sublethal (SL) dose levels. Cythion at SL and Hexadrin at both the concentrations reduced pituitary and serum TSH content. Pituitary TSH levels were unaffected by Cythion at SC dose although serum TSH was effectively brought down. These pesticides probably reduce TSH output which in turn affects thyroid activity or they may directly act on thyroid gland to suppress thyroidal activity on the one hand and interfere with TSH secretion on the other.

Human thyroid stimulating activity and clinical state in antithyroid treatment of juvenile Graves' disease.

Abstract. Human thyroid stimulating activity in 37 patients with juvenile hyperthyroidism was studied during the course of antithyroid drug treatment. Observation periods varied from 6 months to 6 years (average 3 years). The existence of human thyroid stimulator (HTS) in their sera was determined by triiodothyronine (T3) release from resected thyroid adenomas. A measurement of T3 above the control value of 140% was judged to be positive. Before treatment, 25 of the 28 patients with Graves' disease had HTS in their sera, one of the 7 patients with Hashimoto's thyroiditis had HTS, and none of the 19 normal children had HTS in their sera. During the therapy, 7 of 18 Graves' patients had HTS. After cessation of the therapy, 9 of 22 patients remained HTS-positive, and 8 of the 9 patients with positive HTS relapsed within 6 months, whereas in 13 HTS-negative patients, 3 escaped and 10 remained in remission. There was no significant correlation between human thyroid stimulating activity (HTSA) and the following: serum T3 concentration, 131I-thyroidal uptake, TSH responsiveness to TRH and antithyroid antibody titre. These results indicate that (1) almost all patients with Graves' disease have HTS when they are in a state of hyperthyroidism, (2) HTS tends to disappear with the clinicial remission, but its persistence seems to predict relapse in the future, and (3) routine laboratory tests cannot serve as alternative to HTS.

Thyrotrophin binding inhibiting immunoglobulins in Graves' disease before, during and after antithyroid therapy, and its relation to long-acting thyroid stimulator.

Thyrotrophin binding inhibiting immunoglublins (TBII) were measured in twenty-five patients with unequivocal hyperthyroid Graves' disease with a radioreceptor assay for TSH before, during and the end of treatment with antihyroid drugs and triiodothyronine. To assess the outcome of this therapy patients were followed for 10--90 months (mean 63 months). Before treatment there was significant correlation between TBII activity and serum thyroxine (r = -0.48, P less 0.05) and between TBII activated and 24 hour 131I thyroid uptake (r = -0.57, P less than 0.01). No relationship was found between TBII activated and 20 min, 4 hour and 48 hour 131I thyroid uptakes before institution of therapy. During treatment a significant correlation between TBII index and 20 min 131I thyroid uptake was found (r = -0.55, P less than 0.001). Both before and during treatment there was a significant correlation between TBII and LATS activity (r = -0.65, P less than 0.001). From the magnitude of this correlation coefficient it can be concluded that related, although not the same immunoglobulins, are measured with the two assay techniques. It is not possible to predict the occurrence of a relapse from the presence or absence of TBII activity at the end of treatment in this group of patients. The relapse rate was four out of eight for patients without TBII activity in their serum at the end of treatment and five out of nine for patients with TBII activity. From the data presented it can be concluded that although there is a significant relation between TBII activity and some indices of thyroid function before and during treatment, the correlation coefficients are too small to conclude that TBII alone is responsible for the hyperfunction of the thyroid. The same conclusion can be drawn from the fact that TBII activity has no prognostic value in relation to a possible relapse.

A thyroid stimulation test with urinary T3 concentration as an index of thyroid response (author's transl)

Ten U.S.P. of TSH (Thytropar) was administered intramuscularly for three days to five euthyroid controls, to thirteen patients with chronic thyroiditis (four clinically euthyroid patients with normal serum TSH-Group I, five clinically euthyroid patients with high serum TSH-Group II, four clinically hypothyroid patients with high serum TSH-Group III), and to five patients with thyroidal hypothyroidism.Thyroidal 24hr uptake of 131I, 24hr urinary T3 and serum T3 levels were measured.In the euthyroid controls, the basal urinary T3 value was 0.76±0.26 (mean±S.D.) pg/day and increased to 1.31±0.16 on the first day, to 2.33±0.75μg/day on the second day, and to a maximum of 2.78±0.65μg/day on the third day after the TSH administration.In Group I, basal urinary T3 was normal at 0.58±0.16μg/day. Following the TSH administration, the value increased to a maximum of 1.60±0.62/μg/day, but the increase rate was less than that in the euthyroid controls. In Group II, basal urinary T3 was normal at 0.71±0.37μg/day. Following the TSH administration, however, this value did not increase. In Group III, basal urinary T3 was significantly low at 0.32±0.07μg/day, and this value did not increase after the TSH administration.In the thyroidal hypothyroid patients, basal urinary T3 was 0.12±0.10μg/day and lower than that of Group III, and it did not increase after the TSH administration.Positive correlations were found between urinary T3 and serum T3 before and after the TSH administration.In contrast to basal serum T3 and urinary T3, the mean basal thyroidal uptake of 131I in patients with chronic thyroiditis was higher than that of the euthyroid controls. However a positive correlation was found between the increase rate of urinary T3 and that of the thyroidal uptake of 131 I after TSH administration.These observations indicate that the changes in concentration of urinary T3 are reliable indices of thyroidal response to TSH administration in various states of thyroid function.

A study of thyroid reserve in Hashimoto's disease (author's disease)

A three-day thyroid stimulating hormone (TSH) test of administering 10 U.S.P. bovine TSH intramuscularly was performed on 6 normal subjects, 14 patients with Hashimoto's disease and 6 patients with primary hypothyroidism. The response of 24hr thyroidal 131I-uptake (131-uptake) and of serum thyroxine (T4) and triiodothyronine (T3) was studied in these subjects. Of the 14 patients with Hashimoto's disease, T4, T3 and TSH were normal in 5 patients (group 1); both T4 and T3 were normal and TSH was high in 5 patients (group 2); and either both T4 and T3 or one of them was low and TSH was high in 4 patients (group 3); 131I-uptake was normal in groups 1 and 2, and low in group 3. The mean increase in 131I-uptake was 33.7 +/- 11.4% (S.D.) in normal subjects, 22.8 +/- 5.6% in group 1, 4.4 +/- 5.0 in group 2, and no change in group 3 and primary hypothyroidism. The increase in T4 was 9.1 approximately 17/2 microgram /100ml in normal subjects, 3.7 approximately 6.1 microgram/100ml in group 1, 0 approximately 3.2 microgram/100ml in group 2, and no change in group 3 and primary hypothyroidism. Group 2 proved to be in the so-called condition of "low thyroid reserve" because 131I-uptake, T4 and T3, though normal before the test, failed to respond to TSH-stimulation, and endogenous TSH was increased in this group. in group 1, 131I-uptake responded to TSH-stimulation normally, but T4 and T3 did not. Group 1 seemed to be in the early stage of "low thyroid reserve".

Iodoamino acid synthesis in thyroid lobes in vitro with excellent yield of iodothyronines.

Thyroid lobes of male Sprague-Dawley rats on an iodine-sufficient diet were incubated in our improved in vitro system with 0.01 microM 127I and 5mU/ml of bovine TSH. Thyroidal 131I-uptake and the relative incorporation of iodine into iodothyronines increased with time. The average yield of each iodoamino acid after 8 h of incubation was: monoiodotyrosine 28.0%, diiodotyrosine 46.5%, triiodothyronine 1.9% and thyroxine 13.9%, which showed a striking resemblance to the values obtained in vivo. The yields of iodotyrosines and iodothyronines, the latter in particular, were strikingly high, and this system is considered to be useful in the study of thyroidal iodine metabolism. Effects of TSH, temperature and pH of the medium were examined and a unique effect of pH was observed on the iodoamino acid synthesis. As the pH was elevated from 6.8 to 7.9, 131I-uptake, MIT/DIT ratio, T4/DIT ratio and T3/T4 ratio increased. The effect of slightly alkaline pH was considered to be similar to that observed in iodine-deficiency. It was found that the rubber stoppers which are commonly used in short-term incubation contain a kind of potent inhibitor of thyroid hormone synthesis. The pattern of inhibition was similar to that of thionamide compounds.

Trypsin inhibitor, mineral availability, and performance of broiler chickens fed on diets based on rice bran

Trypsin inhibitor in rice bran was inactivated by moist heat, but not by dry heating or treatments with 0.1% H 2SO 4, 0.1% NaOH or 0.1% NaCl. Heating rice bran could not improve its growth promotion value in the diet of broilers, which was related to the feed intake. Groundnut meal was the major protein supplement in the diets. Rice bran diets did not affect weight of pancreas (1.45–1.50 g/kg body weight). Use of 45Ca revealed that availability of calcium on a rice bran diet was lower than on a maize-based diet. A similar effect on 59Fe-availability was noted, although this result needs confirmation. Lack of differences in weight of thyroid glands and uptake of 131I by thyroids of birds on maize- and rice bran-based diets indicated the absence of any goitrogenic substance in the rice bran.

Dissociated thyroxine, triiodothyronine and reverse triiodothyronine levels in patients with familial goitre due to iodide organification defects.

The thyroid function of patients with three different types of organification defect was studied. All patients were characterized by a high thyroidal 131I uptake and a positive perchlorate discharge. Patients with Pendred's syndrome who had goitre and congenital nerve deafness were mostly euthyroid with normal circulating thyroid hormone levels. Only two of them had compensated euthyroidism with elevated total T3, high basal TSH and delayed return to basal value with TRH. The patients who were euthyroid with large goitres and normal hearing had elevated total T3 and an exaggerated TSH response to TRH. The thyroid function of these two groups of patients contrasted with that of goitrous cretins, who were clinically hypothyroid with low circulating total T4, increased T3 and decreased rT3 levels. The data suggest that in patients with intrathyroidal iodine deficiency secondary to organification defect, there is preferential T3 production in an effort to maintain euthyroid state, and this is further substantiated in the case of gross thyroid insufficiency either by enhanced peripheral conversion of T4 to T3, or reduced metabolic clearance of T3 and increased clearance of rT3, resulting in elevated T3 and decreased rT3 levels.

Abnormal Thyroid Regulation in Chickens with Autoimmune Thyroiditis*

The obese strain of chicken (OS) in which virtually all individuals spontaneously develop autoimmune thyroiditis was developed by selection from the Cornell strain (CS). Lymphocytes start infiltrating the thyroid gland 1 week after hatching. One possibility explaining this infiltration postulates preexisting abnormalities or defects of the target organ. The present study examines one parameter of thyroid function, uptake of 131I- under conditions in which TSH secretion is minimized. This was accomplished by supplementation of feed with T4 from hatching until sacrifice. Serum T4 levels were monitored by RIA. Twenty-hour thyroidal iodide uptakes were determined at autopsy by counting the radioactivity in the extirpated thyroid lobes. Dietary T4 supplementation increased serum T4 levels many times above normal. This drastically decreased thyroid function in four normal chicken strains; thyroidal uptake of 131I- was suppressed 97.5-99.2%. OS chickens were incompletely suppressed; mean values ranged between 80...

The effect of mercuric chloride on thyroid function in the rat

Oral administration of 3 mg of mercuric chloride for 6 consecutive days increases thyroid function as noted by an increase in thyroid 131I release rate. Administration of 2.5 mg of mercuric chloride daily for 40 days enhanced thyroid weight, thyroidal 125I uptake, and serum PB125I. Chromatographic analysis of thyroid pronase hydrolysates of mercury-treated rats displayed a pattern of distribution in thyroid labeling which demonstrated an increased percentage of labeled monoiodotyrosine (MIT), no alteration in percentage of labeled diiodotyrosine (DIT) or T4, but a significant reduction in percentage of labeled T3 indicating perhaps a coupling defect in synthesis of T3 exerted by mercury. Administration of mercuric chloride at 100 ppm for 3 months results in a decrease in thyroidal 131I uptake and depression in the thyroidal 131I release rate which were permanent and irreversible. These findings indicate that the influence of mercuric chloride ingestion on thyroid function probably reflects the quantity of mercuric chloride administered and the length of time during which exposure to mercury persists.

Hypothalamo-adenohypophyseal-thyroid interrelationships in the chick embryo: II. Effects of thiourea treatment of plasma total thyroxine levels and thyroidal 125I uptake

After thiourea administration to chick embryos on Day 5.5, total plasma thyroxine concentrations were significantly decreased on Days 7.5, 9.5, 10.5, and 11.5 of incubation. Also, radioiodide uptake in normal and thiourea-treated embryos was measured at 1.0, 3.0, and 5.0 hr post-treatment on all days studied. There was no statistically significant difference in radioiodide uptake between normal and goitrogen-treated embryos on Days 7.5 and 9.5. However, on Days 10.5 and 11.5, a statistically significant increase in radioiodide uptake was observed in thiourea-treated individuals as compared to nontreated embryos. Thyroid wet weights were compared between normal and thiourea-treated embryos on all days studied. There were no statistically significant differences in wet weights between normal and goitrogen-treated individuals on the days assayed. The data indicate that on Day 10.5 of incubation, the pituitary and/or hypothalamus of the chick embryo first responds to decreases in circulating T 4 levels. Thus, the maturation of the hypothalamo-adenohypophyseal-thyroid axis during Days 10.0–13.0 of development in the chick embryo may be similar to that found in sheep and humans at midgestation.

Effects of Rapeseed Meal on Growth and Thyroid Function of Broiler Chicks

Effects of rapeseed meal on growth and thyroid function of broiler chicks were investigated using three types of rapeseed meal, B. campestris, B. napus and B. napus cv. Bronowski. Goitrin and isothiocyanate contents were 0.18 and 0.04% in B. napus cv. Bronowski (RSM-B), 0.28 and 0.18% in B. campestris (RSM-C), and 0.89 and 0.27% in B. napus (RSM-N), respectively. Each RSM was included at the 10% level, and diets were maintained isocaloric and isonitrogenous by altering the levels of soybean meal and yellow grease. The results obtained were summarized as follows:1) Body weight at 4 and 8 weeks of age and feed conversions in chicks fed rapeseed meal were almost equal to those in the control chicks fed soybean meal.2) Thyroid weight of chicks fed rapeseed meal was 1.3 to 3.0 times larger than that of the control chicks. Enlargement of thyroid in chicks fed RSM-N, which contained 0.89% goitrin, was particularly noteworthy.3) Thyroidal uptake of 131I (24 hours) of rapeseed meal-fed chicks was elevated 1.1 to 2.3 times that of the control group. Thyroidal uptake of 131I per 100mg of the thyroid gland, however, was not affected by rapeseed meal feeding.4) Plasma PB 131I, which reflects circulating level of thyroid hormone, seemed to be not or to be very slightly depressed by rapeseed meal feeding.5) Percentage of 131I-iodothyronines in the thyroid lobes was slightly decreased by feeding of rapeseed meal. However, the content of PAS-stainable (thyroglobulin) in the follicles of the thyroid lobes of chicks fed rapeseed meal was similar to that of the control chicks.6) It was concluded in this experiment that thyroid function in chicks fed rapeseed meal was kept fairly good, despite of the enlargement of thyroid gland.