Effects of a diet plus exercise program on thyroid function in patients with obesity
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Studies of thyroid function after diet-induced weight loss in patients with obesity have yielded conflicting results. It is not known whether adding exercise to diet affects thyroid function in this patient population. The aim of the study was to prospectively evaluate the effects of a rehabilitation program on weight, body composition and thyroid function in euthyroid patients with obesity.Serum levels of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and free triiodothyronine (FT3) in euthyroid patients with severe obesity were analyzed before and at the end of a 3-month rehabilitation program. Relationships between body weight or composition and changes in thyroid function were also investigated. Each study participant acted as his/her own control.The study population consisted of 34 euthyroid patients with obesity (18 men and 16 women; mean ± SD age: 51 ± 12). The mean BMI was 49.3 ± 12.4 kg/m2 before the program and 46 ± 10.8 (p < 0.005) at the end, with a mean body weight loss of 11 kg (p < 0.05) and a mean fat mass loss of 6.8 kg (p < 0.05). The weight and fat mass losses were not significantly correlated with the serum concentrations of TSH, FT3 and FT4 measured at the end of the program.A 3-month rehabilitation program combining diet and exercise produced weight and fat mass losses without inducing thyroid dysfunction in patients with obesity.SUMMARY Total and free serum thyroxine (T4) and triiodothyronine (T3), basal serum thyrotrophin (TSH) and the serum TSH response to a standard intravenous dose of thyrotrophin releasing hormone (TRH) have been measured in fifteen men with liver cirrhosis and in eight alcoholic men with fatty liver change. All the patients studied were clinically euthyroid. In cirrhotics, total T4 and free T4 (FT4) concentrations were normal as were free T3 (FT3) concentrations but total T3 concentrations were significantly reduced and basal TSH concentrations were significantly higher than normal. Alcoholics with fatty liver change had normal basal TSH concentrations and normal total and free thyroid hormone concentrations apart from reduced FT4. Correlation of thyroid function tests with liver function (serum albumin concentration) showed significant positive correlations for serum albumin with both total T3 and FT3 and significant negative correlations with both FT4 and basal TSH. Nine of fifteen cirrhotics had an abnormal serum TSH response to TRH, the commonest abnormal pattern being a delayed response (seven patients). Three of eight alcoholics with fatty liver change also had an abnormal TSH response to TRH. These findings not only show complex disturbances in hypothalamic‐pituitary‐thyroid relationships in chronic liver disease but also provide indirect evidence of reduced extra‐thyroidal conversion of T4 to T3.
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Thyroid-stimulating hormone
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Free thyroxine
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TRH stimulation test
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Coturnix
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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.
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Myxedema
Reverse triiodothyronine
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Congenital hypothyroidism
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Abstract. The plasma concentrations of thyroxine (T 4 ), free thyroxine (free-T 4 ), triiodothyronine (T 3 ), reverse triiodothyronine (rT 3 ), TSH and thyroxine-binding globulin (TBG) were measured in 19 children suffering from idiopathic growth hormone deficiency. Blood was taken before and one month after growth hormone treatment. Ten patients were hypothyroid (group 1) and 9 were euthyroid (group 2). The basal T 3 and rT 3 levels correlated well with the T 4 concentrations. Free-T 4 levels were very low in all the hypothyroid patients and proved to be the most reliable index of TSH deficiency. TBG concentration was high in the hypopituitary patients regardless of their thyroid function. Following growth hormone treatment T 4 , free-T 4 and rT 3 levels fell in both groups. The T 3 concentration rose in group 1 but no change was seen in group 2. There was a significant correlation between the changes of T 4 and T 3 , such that the increase in T 3 level was greatest in those with only a slight reduction of T 4 concentration and no T 3 increase was seen with more marked T 4 decreases. The plasma TBG concentration is enhanced in growth hormone deficiency causing relatively high T 4 values. Growth hormone treatment reduces T 4 secretion and affects the peripheral metabolism of thyroid hormones resulting in an increase of T 3 and a reduction of rT 3 concentration.
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We studied the effect of short-term triiodothyronine administration on thyroid gland responsivity to exogenous thyrotropin in four euthyroid human subjects. Thyroidal iodine release and serum thyroxine during daily im injections of bovine TSH were not significantly inhibited, despite a fourfold elevation in serum TMs3 concentrations. This negative finding contrasts with earlier positive reports of a regulatory “short-loop” effect of elevated circulating T3 on the thyroid gland. This difference may be due either to the use in previous murine or in vitro studies of non-physiologic, high doses of exogenous T3, or failure to control the withdrawal of the trophic effect of endogenous TSH in man on the subsequent glandular response.
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Adipose tissue is a hormonally active system that produces and releases different bioactive substances. Leptin, adiponectin and resistin are some of the recently discovered adipocytokines that participate in the regulation of intermediate metabolism. The aim of this study was to evaluate the circulating levels of leptin, adiponectin and resistin in patients with thyroid dysfunction before and after normalization of thyroid function with appropriate therapy.We studied 20 patients with hyperthyroidism (16 women and 4 men; mean age 47.2 +/- 3.9 years) and 20 patients with hypothyroidism (17 women and 3 men; 51.5 +/- 4.1 years). A group of 20 euthyroid subjects served as control group. Patients were evaluated at the time of diagnosis and again after normalization of thyroid function with appropriate therapy. Serum concentrations of free T4 (FT4), total T3, TSH, insulin, leptin, adiponectin and resistin were measured in all subjects.Hyperthyroid patients showed significantly decreased leptin levels in comparison with controls (11.0 +/- 1.1 vs. 30.4 +/- 5.0 microg/l, P < 0.001). No significant differences in adiponectin levels between hyperthyroid and control groups were found (27.8 +/- 4.0 vs. 46.0 +/- 12.0 mg/l, NS). Patients with hyperthyroidism exhibited reduced resistin levels in comparison with euthyroid subjects (6.4 +/- 0.8 vs. 8.4 +/- 0.7 microg/l, P < 0.05). Normalization of circulating thyroid hormone was accompanied by a nonsignificant increase in leptin levels (12.9 +/- 1.7 microg/l, P < 0.01 vs. control) and no significant modification both in adiponectin (32.0 +/- 7.1 mg/l, NS) and resistin (5.4 +/- 0.7 microg/l, NS) levels. Adjustment of adipocytokine concentrations for body mass index (BMI) showed that treatment of hyperthyroidism induced a significant reduction in adjusted resistin concentrations (0.21 +/- 0.03 vs. 0.28 +/- 0.03 microg/l/BMI units, P < 0.05), with no changes in adjusted leptin and adiponectin. Hypothyroid patients showed significantly lower leptin levels compared with the controls (16.0 +/- 3.5 vs. 30.4 +/- 5.0 microg/l, P < 0.05). Adiponectin levels in patients with hypothyroidism (71.8 +/- 16.0 mg/l) were similar to those in the control group and were not modified with therapy. Resistin levels were significantly reduced among hypothyroid patients (5.8 +/- 1.0 microg/l, P < 0.05), and were not increased after levothyroxine therapy. A significant rise in BMI-corrected leptin levels was observed after replacement therapy, with no changes in adiponectin- and resistin-corrected values.The results suggest that (1) low serum leptin levels are present in both hyperthyroid and hypothyroid patients but are only increased after therapy in the latter; (2) resistin might be implicated in the insulin resistance state that accompanies thyrotoxicosis; and (3) inadequate secretion of adiponectin seems to have no role in metabolic changes associated with thyroid dysfunction.
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The pituitary-thyroid axis was investigated in nineteen euthyroid patients with severe diabetic ketoacidosis. A 'low T3 syndrome' was found, with the following characteristics: lowered serum concentrations of triiodothyronine (T3), increased reverse triiodothyronine (rT3), slightly low thyroxine (T4), normal thyrotrophin (TSH), slightly increased triiodothyronine uptake (RT3U) values, and a blunted TSH response to thyrotrophin-releasing hormone (TRH). These disturbances in thyroid-function tests required several days good control of the diabetes to be corrected, at least partially. The data suggest the presence of an abnormal extrathyroidal T4 metabolism as well as a pituitary defect. Caution is recommended in the interpretation of thyroid-function tests during and several days after the treatment of diabetic ketoacidosis.
Diabetic ketoacidosis
Reverse triiodothyronine
Ketoacidosis
Euthyroid sick syndrome
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The plasma concentrations of thyroxine (T4), free thyroxine (free-T4), triiodothyronine (T3), reverse triiodothyronine (rT3), TSH and thyroxine-binding globulin (TBG) were measured in 19 children suffering from idiopathic growth hormone deficiency. Blood was taken before and one month after growth hormone treatment. Ten patients were hypothyroid (group 1) and 9 were euthyroid (group 2). The basal T3 and rT3 levels correlated well with the T4 concentrations. Free-T4 levels were very low in all the hypothyroid patients and proved to be the most reliable index of TSH deficiency. TBG concentration was high in th hypopituitary patients regardless of their thyroid function. Following growth hormone treatment T4, free-T4 and rT3 levels fell in both groups. The T3 concentration rose in group 1 but no change was seen in group 2. There was a significant correlation between the changes of T4 and T3, such that the increase in T3 level was greatest in those with only a slight reduction of T4 concentration and no T3 increase was seen with more marked T4 decreases. The plasma TBG concentration is enhanced in growth hormone deficiency causing relatively high T4 values. Growth hormone treatment reduces T4 secretion and affects the peripheral metabolism of thyroid hormones resulting in an increase of T3 and a reduction of rT3 concentration.
Reverse triiodothyronine
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Free thyroxine
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The regulatory role of thyroid hormone on the adenyl cyclase-adenosine 3′,5′-monophosphate (cyclic AMP) system in human thyroid slices and plasma membranes from euthyroid subjects and thyrotoxic patients were studied by measuring the formation and accumulation of labeled and cold cyclic AMP. TSH stimulated adenyl cyclase-cyclic AMP system of the thyroid from euthyroid subjects and thyrotoxic patients, but the response was less in the thyroid from thyrotoxic patients. Small (10−9M) or large (10−4M) doses of thyroxin (T4) and triiodothyronine (T3) decreased the TSH-stimulated elevation of labeled and cold cyclic AMP level in the thyroid from euthyroid subjects. In contrast, graded doses of T4 (10−5 to 10−8M) and T3 (10−6 to 10−7M) failed to depress TSH-stimulated elevation of 3H cyclic AMP level in the thyroid from thyrotoxic patients. Large doses of T4 (10−4M) and T3 (10−4 and 10−5M) depressed TSH-stimulated adenyl cyclase activity, however. Since large doses of iodide and d-T4 have no effect on adenyl cyclase activity of the thyroid, and since T4 did not affect cyclic AMP accumulation of fat pads produced by catecholamine, it is suggested that thyroid hormones play an important role for the control of thyroid function through the depression of thyroidal adenyl cyclase-cyclic AMP system activated by TSH.
Thyroid-stimulating hormone
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