T3 Resin Uptake Research Articles

Thyroid Hormone Economy in Response to Extreme Cold Exposure in Healthy Factory Workers*

The effects of cold exposure on serum total T4 (TT4), total T3 (TT3), free T4 (FT4), free T3 (FT3), rT3, TSH, T4-binding globulin (TBG), and T3 resin uptake were investigated in 82 euthyroid factory workers. Twenty-five workers (group 1) were exposed intermittently (approximately 3.5 h daily) to extreme cold (-40 to -20 C) during the 8-h work shift, and 47 (group 2) were exposed to moderate cold (-10 to 8 C) for the entire 8 h. Ten individuals working at room temperature for the same period also were studied. After cold exposure, serum TT4 decreased in group 1 and did not change in group 2, whereas FT4 did not change in group 1 and increased in group 2. After exposure, serum TT3 and rT3 decreased significantly in both groups, while FT3 did not change in either. The basal serum TT4 levels in groups 1 and 2 were significantly lower than those in the control group, whereas those of FT4 and FT3 were higher. Thus, cold exposure had opposite effects on total thyroid hormones and their free fractions, consistent with a cold-induced decrease in thyroid hormone-binding capacity. A postexposure decrease in serum TBG was found in women in group 2, but not in men in either group 2 or group 1, suggesting that factors other than decreased TBG are also involved. The results suggest the possibilities that 1) decreased thyroid hormone-binding capacity is an adaptive response to cold exposure, and/or 2) increased free thyroid hormone levels in response to cold exposure result in a new higher equilibrium between extracellular and intracellular FT4 and FT3.

Decline of T3 and elevation in reverse T3 induced by hyperglucagonemia: changes in thyroid hormone metabolism, not altered release of thyroid hormones.

Recently we reported that hyperglucagonemia induced by glucagon infusion causes a decline in serum Triiodothyronine (T3) and a rise in reverse T3 (rT3) in euthyroid healthy volunteers. These changes in T3 and rT3 levels were attributed to altered T4 metabolism in peripheral tissues. However, the contribution of altered release of thyroid hormones by the thyroid gland could not be excluded. Since the release of thyroid hormones is suppressed by exogenous administration of L-thyroxine (L-T4) in appropriate dosage, we studied thyroid hormone levels for up to 6 hours after intravenous administration of glucagon in euthyroid healthy subjects after administration of L-T4 for 12 weeks. A control study was conducted using normal saline infusion. Plasma glucose rose promptly following glucagon administration demonstrating its physiologic effect. Serum T4, Free T4 and T3 resin uptake were not altered during both studies. Glucagon infusion induced a significant decline in serum T3 (P less than 0.01) and a marked rise in rT3 (P less than 0.01) whereas saline administration caused no alterations in T3 or rT3 levels. Thus the changes in T3 and rT3 were significantly different during glucagon study when compared to saline infusion. (P less than 0.01 for both comparisons). Therefore, this study demonstrates that changes in serum T3 and rT3 caused by hyperglucagonemia may be secondary to altered thyroid hormone metabolism in peripheral tissues and not due to altered release by the thyroid gland, since the release of thyroid hormones is suppressed by exogenous L-T4 administration.

Thyroid hormone indices in adult healthy subjects: no influence of aging.

Controversy exists regarding the influence of aging on thyroid hormone metabolism. Several investigators report lowering of T3 and/or a rise in reverse T3 (rT3) in elderly subjects. Others suggest that these thyroid hormone alterations were secondary to associated disorders rather than old age, and questioned the "healthy" status of the subjects studied in the earlier reports. Therefore, to assess the possible effect of aging we studied T3 resin uptake, T4, free T4, T3, and rT3 concentrations in 152 euthyroid healthy adult subjects. These subjects were selected carefully and were therefore devoid of any illness, acute or chronic, and were not treated with any medications at the time of study. No significant alterations were noted in any of the thyroid hormone concentrations in subjects divided into groups according to age. Nor was there a significant difference in these parameters between men and women of any individual age group or for all ages combined. Therefore, old age per se may not influence thyroid hormone metabolism and hence may not induce changes in serum thyroid hormone concentrations. The changes in thyroid hormones noted previously in elderly subjects may be a reflection of concurrent disorders and not old age.

Measurement of T4, T3 and reverse T3 levels, resin T3 uptake, and free thyroxin index in blood from the intervillous space of the placenta, in maternal peripheral blood, and in the umbilical artery and vein of normal parturients and their conceptuses.

T4, T3, and reverse T3 (rT3) levels and the free thyroxine index were measured in blood collected from the intervillous space (IVS) after placental expulsion and compared to the values in maternal peripheral blood and in umbilical artery and umbilical vein of 21 clinically normal parturients and their conceptuses. T4 levels in maternal peripheral blood did not differ significantly from T4 levels in the IVS, but were significantly higher than those detected in umbilical vein and artery (p less than 0.05). There was no difference in T4 levels between umbilical vein and artery. The free thyroxine index was similar for the maternal compartments (maternal peripheral blood and IVS), but differed significantly from the fetal compartments (umbilical vein and umbilical artery). T3 levels in maternal peripheral blood were significantly higher than in the IVS, both of these values being significantly higher than in the fetal compartments. There was no difference in T3 levels between umbilical vein and artery. rT3 levels of maternal peripheral blood were one third that of the IVS (p less than 0.05). rT3 levels of the umbilical vein were 1.5 times higher than those of the IVS (p less than 0.05) and 5.2 times higher than those of maternal peripheral blood (p less than 0.005). No significant difference was obtained between umbilical vein and artery. The increase in rT3 and the decrease in T3 in the IVS in relation to maternal peripheral blood support the hypothesis that the placenta may preferentially convert T4 to rT3 at the expense of T3. The present data, however, do not permit the identification of the site where this conversion takes place.

Lowering of T3 and rise in reverse T3 induced by hyperglucagonemia: altered thyroid hormone metabolism, not altered release of thyroid hormones.

Recently we reported that hyperglucagonemia induced by glucagon infusion causes a decline in serum T3 and a rise in reverse T3 in euthyroid healthy volunteers. These changes in T3 and rT3 levels were attributed to altered T4 metabolism in peripheral tissues. However, the contribution of altered release of thyroid hormones by the thyroid gland could not be excluded. Since the release of thyroid hormones is inhibited in primary hypothyroidism and is almost totally suppressed following L-thyroxine replacement therapy, we studied thyroid hormone levels for up to 6 hours after intravenous administration of glucagon in subjects with primary hypothyroidism who were rendered euthyroid by appropriate L-thyroxine replacement therapy for several years. A control study was conducted using normal saline infusion. Plasma glucose rose promptly following glucagon administration demonstrating its physiologic effect. Serum T4, Free T4, and T3 resin uptake were not altered during both studies. Glucagon infusion induced a significant decline in serum T3 (P less than 0.05) and a marked rise in rT3 (P less than 0.05) whereas saline administration caused no alterations in T3 or rT3 levels. Thus the changes in T3 and rT3 were significantly different during glucagon study when compared to saline infusion. (P less than 0.01 for both comparisons). Since, the release of thyroid hormones is suppressed by exogenous LT4 administration in these subjects; we conclude that changes in serum T3 and rT3 observed following glucagon administration reflect altered thyroid hormone metabolism in peripheral tissues and not altered release by the thyroid gland.

Lowering of serum T3 and rise in reverse T3 induced by glucagon infusion in anaesthetized dogs.

We recently demonstrated that lowering of T3 and a rise in rT3 observed in non-thyroidal illnesses could be induced by glucagon infusion in normal subjects without altering T4. Free T4 (FT4) and T3 resin uptake (T3RU) values suggesting that altered T4 metabolism may be mainly responsible for those changes. To further assess the role of altered T4 metabolism in these changes during induction of hyperglucagonaemia, we studied glucose, T4, FT4, T3RU, T3, and rT3 concentrations before and after iv glucagon injection (0.5 mg) for up to 3 h in 6 anaesthetized dogs, since thyroxine-binding globulin (TBG) concentration is known to be extremely low in dogs. A control study was conducted with iv normal saline (0.5 ml) injection. T4, FT4 and T3RU remained unchanged during both studies. A significant fall was noted in T3 with glucagon (delta T3, 0.23 +/- 0.06 nmol/l vs 0 +/- 0.03 nmol/l with normal saline; P less than 0.01). rT3 rose markedly following glucagon infusion (delta rT3, 0.04 +/- 0.011 nmol/l vs -0.017 +/- 0.006 nmol/l with normal saline; P less than 0.01). Moreover, areas under the curves for T3 and rT3 were markedly increased during glucagon infusion when compared to saline administration (P less than 0.01 for both comparisons). Therefore, this study suggests that changes in T3 and rT3 concentrations observed in non-thyroidal illnesses may be attributed to hyperglucagonaemia and may be secondary to altered T4 metabolism as reflected by lowered T3/T4 and increased rT3/T4 ratio.

Effect of oral frusemide on diagnostic indices of thyroid function.

We studied the acute effect of standard therapeutic doses of oral frusemide on indices of thyroid function in 34 hospital in-patients with congestive cardiac failure. A transient decrease in total T4, elevation in the T3 resin uptake and consequent increase in the free T4 index (FT4I) were seen 2-5 h after ingestion of frusemide at a chronic morning dosage of 80, 120 or 250 mg. The FT4I pre-vs post-frusemide values after 250 mg of drug were 109 +/- 12 vs 129 +/- 18 (P less than 0.05) after 120 mg 92 +/- 14 vs 119 +/- 12 (P less than 0.01), and after 80 mg 102 +/- 6 vs 112 +/- 4 (P less than 0.01) (mean +/- SEM). Similar increases in apparent free T4 measured by an analogue tracer assay (free T4 RIA sol, Henning, Berlin) were seen after frusemide. In a time course study, the major change in the T3 uptake 120 min after frusemide ingestion correlated with the change in serum frusemide concentration. When frusemide was added to serum in vitro its influence was greatest in methods that involved least dilution of serum. In two of the patients difficulty in clinical assessment of thyroid status was compounded by the effect of oral frusemide on FT4I. We conclude that oral frusemide may influence biochemical assessments of thyroid function in patients with congestive cardiac failure. It is necessary to consider the time interval between ingestion of high doses of oral frusemide and blood sampling in evaluating such results.

Fonction thyroïdienne du brûlé : Incidence de la thérapeutique iodée

Thyroid function was studied in 3 groups of adults (group I = 13 burned patients treated with non iodinated antiseptic, group II = 15 burned patients treated with polyvidone iodine, group III = 50 control subjects) in order to examine: the thyroid hormone status in burned patients, the possible incidence of plasma iodine overload on these endocrine parameters. Burned skin area and thyroid function were measured before treatment, then weekly for 3 weeks. Before treatment a decrease in plasma T4 and T3 with an increase in reverse T3 (rT3) and a decrease in plasma thyroxin binding globulin (TBG) were observed in burned patients. Free T4 index (T4/TBG) was normal, but T3 resin uptake (T3RU) was elevated. During treatment, plasma iodine increase sharply from 6.4 +/- 0.4 to 20.7 +/- 4.7 micrograms/100 ml (p less than 0.02) in group II. Endocrine parameters (not different between group I and II) progressively returned to normal, except for T3RU which remained elevated until the third week. rT3, T4 and T3RU correlated (p less than 0.001) with burned skin area. To conclude, the reversible particularities of thyroid function in burned patients are positively correlated with burned area. The thyroid function does not seen to be modified by plasma iodine overload.

Relationship between thyroid hormones and nutrition in chronic renal failure.

A cross-sectional study was performed in 19 patients on haemodialysis and in 11 on continuous ambulatory peritoneal dialysis (CAPD) in order to investigate the relationship between thyroid hormones and nutritional status. T4, T3 resin uptake, T3, rT3 and TSH were measured by radio-immunoassay and compared with controls. Nutritional status was assessed by measurements of blood proteins, albumin, gamma-globulin, transferrin, arm muscle circumference and triceps skinfold thickness. In haemodialysis, T4, FTI, T3 and rT3 were significantly decreased. TSH was normal. In CAPD, thyroid hormones were normal. In both groups, proteins, albumin, gamma-globulin and transferrin were normal. Triceps skinfold thickness was normal in males and females, whereas arm muscle area was dramatically reduced in males and normal in females. In haemodialysis, a negative correlation was found between T3 and proteins (p less than 0.01), rT3 versus proteins (p less than 0.01) and versus gamma-globulin (p less than 0.01). In CAPD, a positive correlation was found between T3 and triceps skinfold thickness (p less than 0.05). We suggest that the overload of carbohydrate might normalize the thyroid hormones in patients on CAPD. The relationship between thyroid hormones and nutritional status in patients treated by dialysis suggests a putative protective effect of low T3 levels against protein breakdown.

Thyroid function tests. Selective use for cost containment.

Clinicians often obtain a variety of thyroid function tests in patients suspected of having thyroid disease when only a few are necessary to adequately establish a diagnosis and do follow-up. For hyperthyroidism and hypothyroidism, measurement of serum T4 is the best screening test. The serum T3 resin uptake test should be added with women suspected of being hyperthyroid because of the changes produced by pregnancy or estrogen-containing contraceptives. Various imaging techniques, including RAI, ultrasound, CT, and MRI, are often used for differentiating benign or cystic thyroid nodules from malignant or solid ones. Each of the available techniques has a different cost, and each is most suitable for a particular disorder. Special tests (eg, TRH testing and measurement of serum TBG) should be added to the basic screening tests only for questionable cases to differentiate diagnostic possibilities or confirm an uncertain diagnosis.

Thyroid-vitamin a interactions in chicks exposed to 3,4,3′,4′-tetrachlorobiphenyl: Influence of low dietary vitamin a and iodine

Poultry chicks receiving a low vitamin A semipurified diet and exposed to 3,4,3',4'-tetrachlorobiphenyl became hypothyroid in comparison with unexposed controls. Metabolic rate, total serum thyroxine, total serum triiodothyronine, and food intake decreased significantly while thyroid weight increased. Unexpectedly, growth rate was not affected on this diet. In the case of chicks receiving a low vitamin A--low iodine semipurified diet and exposed to the PCB congener, the hypothyroid response was apparently antagonized. Comparing exposed chicks with unexposed controls, metabolic rate and the proportion of free T3 (i.e., %T3 resin uptake) increased while total serum thyroxine and thyroid weight were unchanged. In addition, growth rate, food consumption, and serum retinol decreased on this diet. These results are interpreted to mean that growth rate may have been altered by circulating levels of retinol, and vitamin A insufficiency may predispose birds to the hypothyroid effects of PCBs.

Circulating thyroid hormones in primates with mild or severe hepatitis following liver transplantation.

In order to study the effects of acute immunologically mediated liver disease on circulating thyroid hormones, serum levels of thyroxine (T4, total and free) and triiodothyronine (T3) were measured in 8 baboons before and for 60 days after allogeneic liver transplantation. In 3 animals early rejection and jaundice developed; T4 levels declined as liver function deteriorated. In the 5 tolerant animals liver function was only temporarily deranged without jaundice and there was a consistent early rise in T4 (P less than 0.01) followed by a later fall. T3 concentrations were relatively normal in both groups. The T3 resin uptake test remained virtually unchanged in all animals. Serum T4 and T3 responses to exogenously administered bovine thyrotropin (TSH) were similar in the jaundiced and anicteric animals. We conclude that the early rise in T4 in the tolerant animals was caused by transient increases in thyroid binding globulin in (TBG) while the fall in thyroid hormones in these and in the jaundiced animals was related to a decline in TBG levels. Thyroid responsiveness to TSH is not disturbed by moderately deranged liver function.

Pituitary-thyroid function and thyrotropin, prolactin and growth hormone responses to TRH in patients with chronic alcoholism.

Basal plasma concentrations of thyroxine (T4), 3,3',5-triiodothyronine (T3), free T4 index (TF4I), free T3 index (FT3I) reverse T3, 3,3',5-triiodothyronine (rT3), resin T3 uptake (TR3U), thyroxine-binding globulin (TBG), thyrotropin (TSH), prolactin (PRL) and growth hormone (GH) as well as thyrotropin releasing hormone (TRH) stimulated TSH, PRL and GH were investigated in 31 consecutive male patients (mean age 41 years) with chronic alcoholism. According to the histology of their liver biopsies the patients were divided into three groups: patients with normal livers, steatosis and cirrhosis. The control group consisted of 30 healthy males. The patients had abstained from alcohol for at least one week when studied, and they were on a nutritionally adequate diet. All had consumed a daily minimum of 52 g ethanol for at least 5 years. None of the patients had severe or decompensated liver disease. The patients had significantly reduced T3 and rT3 plasma levels compared to normals. Patients with cirrhosis of the liver had increased TBG and normal RT3U levels, while those without cirrhosis had increased RT3U and normal TBG levels. Plasma concentrations of basal as well as TRH-stimulated TSH and PRL were unchanged in alcoholic patients, whereas basal as well as stimulated GH levels were increased in cirrhotic alcoholics. It is concluded that alcohol per se influences T3 levels, but not the part of the hypothalamic-pituitary axis studied, and that the binding proteins are mostly determined by the degree of liver disease.

Glucagon Administration Induces Lowering of Serum T3and Rise in Reverse T3in Euthyroid Healthy Subjects

Euthyroid sick syndrome is characterized by low serum T3 and raised reverse T3 (rT3). Most of the states with this syndrome are also documented to manifest hyperglucagonemia. Furthermore, several recent studies have suggested that glucagon may play a role in T4 monodeiodination in some of these states such as starvation and uncontrolled diabetes mellitus. Therefore, hyperglucagonemia was induced by intravenous glucagon administration in euthyroid healthy volunteers and thyroid hormone levels were determined at frequent intervals up to six hours. Plasma glucose and insulin rose promptly on glucagon administration, thus establishing the physiologic effect of glucagon. Serum T4, free T4, T3 resin uptake, and TSH concentrations remained unaltered throughout the study period. Serum T3 declined to a significantly low level (P less than 0.05) between 60-90 minutes. Serum rT3 rose significantly (P less than 0.05) by four hours and the rise was progressive till the end of the study period. Therefore, these results suggest that hyperglucagonemia may be one of the factors responsible for lowering of T3 and a rise in rT3 in euthyroid sick syndrome.

'Chemical hyperthyroidism': the significance of elevated serum thyroxine levels in L-thyroxine treated individuals.

We have previously reported that L-thyroxine treated patients may often have elevated serum T4 concentrations and yet show no clinical signs of hyperthyroidism. We found that such patients had normal serum T3 concentrations. The present study explored the relationship between serum T3 and T4 and dosage of L-thyroxine. Retrospective analysis of 99 patient records was performed. There was an increase of serum T4, serum T3 resin uptake (T3R), and T3 with increasing dose of L-thyroxine. The T3/T4 ratio decreased with increasing dose of L-thyroxine and with increasing T4. This phenomenon was analysed prospectively by starting 23 individuals on L-thyroxine and progressively incrementing the dose until either symptoms of hyperthyroidism developed or T4 levels exceeded the upper unit of the normal range. Once again, there was a progressive increase in serum T4, T3R, and T3 with increasing dose of L-thyroxine. At even the lowest dose of L-thyroxine (0.05 mg), there was a marked fall in T3/T4 ratio as compared to untreated individuals. The T3/T4 ratio fell further with increasing dose but with a fairly weak correlation. The decrease in T3/T4 ratio showed a much stronger correlation with serum T4. Of the 23 individuals, all exceeded the upper limit of the normal range of serum T4. No individual with elevated T4 developed clinical signs of hyperthyroidism unless serum T3 was also elevated beyond the normal range. Of eight individuals who reached elevated T3 levels, six demonstrated clinical signs of hyperthyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Primary acquired hypoaldosteronism

Primary acquired hypoaldosteronism

A longitudinal evaluation of thyroid function in critically ill surgical patients.

Thyroid hormone alterations (known as the "sick-euthyroid syndrome") are common following major surgery, but the time course for appearance and recovery from these alterations has not previously been longitudinally studied in a large group of surgical patients. The authors prospectively studied 59 patients undergoing major surgery (coronary artery bypass grafting, pneumonectomy, or subtotal colectomy). Compared with preoperative values, the mean serum T4, T3, free T3, and TSH concentrations decreased significantly (p less than 0.05) following surgery. Serum reverse T3 and T3 resin uptake index increased, while free T4 levels remained unchanged. These changes were seen within 6 hours of surgery and normalized by 1 week after surgery. Although the serum TSH response to TRH was normal before and after surgery in 56 of the 59 patients, the maximal TRH-induced increase in serum TSH and the integrated serum TSH response to TRH were suppressed in the early perioperative period. This postoperative TSH suppression correlated with elevated postoperative plasma dopamine concentrations (r = 0.57, p less than 0.05). Three patients with compensated primary hypothyroidism were detected in the study and represent the first documentation of serial thyroid hormone and TSH levels in hypothyroid patients undergoing major surgery. These patients had similar changes in thyroid hormone values compared with euthyroid patients. The serum TSH response to TRH was suppressed into the normal range in two of these patients on the day following surgery. The authors conclude that the sick-euthyroid syndrome occurs within a few hours of major surgery and remits with convalescence. Postoperative decreases in serum TSH may mask the diagnosis of hypothyroidism. Surgical consultants should be aware of these rapid postoperative changes so that thyroid function tests are properly interpreted in patients who have undergone major surgery.

The Gee case: first expert witness.

The Gee case: first expert witness.

新生児,乳児期における甲状腺機能に関する研究

Serum TSH, T4, T3 rT3 and resin T3 uptake (RT3U) were daily or monthly measured in 71 full-term neonates and 146 healthy infants, to study the changes of these thyroid hormones levels in relation to the development during infancy.Serum TSH levels at the first day of life were very high and the geometric mean was 18.8 μU/ml. Following an abrupt fall at the second day (a mean of 7.7 μU/ml), the level decreased gradually to a mean of 3.4 μU/ml at the third week, which was not significantly different from the values in children aged 1 to 5 years.Serum T4 and T7 (T4 x RT3U) values remained high during the first 5 days of life (16.1-18.9 μg/dl for T4 and 5.2-6.4 for T7) as compared with the levels in cord blood. The levels decreased to values similar to those seen in children aged 1 to 5 years by the third week of life (10.8 μg/dl for T4 and 2.9 for T7). Serum T3 levels in the first 2 days of life were high as compared with those of cord blood. Following a transient fall until the age of 4 days, the level again increased slowly and reached the maximum mean level of 208 ng/dl at 3 months. The mean T3 levels between 3 and 21 days of life (113-155 ng/dl) were lower than those in children aged 1 to 5 years (169 ng/dl), but the levels in infants aged 3 to 6 months (190-208 ng/dl) were higher than those in children aged 1 to 5 years. On the other hand, serum rT3 levels were remarkably high in cord blood (184 ng/dl) and remained high during the first 5 days of life (158-231 ng/dl). An abrupt fall occurred at the second week (a mean of 70 ng/dl), and thereafter the levels decreased slowly to a mean of 26 ng/dl by the age of 7 to 8 months, a value similar to that seen in children aged 1 to 5 years.The difference in the T3/T4 ratio from that in children aged 1 to 5 years had become insignificant by the age of 22 to 28 days, while the differences in the rT3/T4 and T3/rT3 ratios had become insignificant by the age of 7 to 8 months.These results suggested that the varying maturation of the conversion mechanism of T4 to T3 in the peripheral tissues in developing infants together with the neonatal surge of TSH secretion may be responsible for these extraordinary changes of serum thyroid hormones during infancy, especially in the neonatal period. The present study also demonstrated that the maturation of the conversion mechanism has completed by the age of 7 to 8 months.

Possible altered dopaminergic modulation of pituitary function in normal-menstruating women with insulin dependent diabetes mellitus (IDDM).

In order to assess whether a possible altered dopamine activity in normal-menstruating diabetic patients may influence the pituitary hormone secretion we have measured the basal serum concentrations of Prl, LH and FSH in 28 patients with insulin dependent diabetes mellitus (IDDM) and in 55 normal-menstruating women at day 3 to 6 of the menstrual cycle. In addition basal levels of oestradiol-17 beta, TSH, thyroxine (T4), triiodothyronine (T3) and resin-T3 uptake (RT3U) were determined in 17 patients with IDDM and in 17 controls. The responses of FSH, LH, Prl, GH and TSH to metoclopramide (MTC) administration (10 mg iv) were studied in 17 patients and 17 controls. In 10 patients with IDDM and 8 controls the short-term variations in pituitary hormones and blood glucose concentration were evaluated. Patients with IDDM had significantly lower basal levels of Prl (P less than 0.01) and TSH (P less than 0.05) and significantly (P less than 0.05) higher basal levels of GH than normal women. No significant (P greater than 0.05) differences were found regarding basal serum concentrations of FSH, LH, oestradiol, T4, T3 and RT3U. During the 3 h period the mean coefficient of variation of Prl, FSH, LH and GH was not significantly (P greater than 0.05) different between diabetic patients and controls. Both groups responded significantly (P less than 0.01) in Prl and TSH to MTC but the TSH response was significantly (P less than 0.05) lower in patients with IDDM. The Prl response to MTC was not significantly (P greater than 0.05) different within the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)