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PubMed1987

Lipid peroxidation and free radical scavengers in thyroid dysfunction in the rat: a possible mechanism of injury to heart and skeletal muscle in hyperthyroidism.

This study was designed to determine if peroxidation of biomembrane lipid and the protective system can be modified by the change in oxidative metabolism induced by thyroid dysfunction. The free radical scavengers (i.e. cuprozinc cytosolic and mangano mitochondrial superoxide dismutases, glutathione peroxidase, and catalase), mitochondrial oxidative marker enzymes (cytochrome c oxidase and fumarase), and lipid peroxide were measured in liver, heart, soleus (slow oxidative), and extensor digitorum longus (fast glycolytic) muscles. Rats were rendered hyper- or hypothyroid for 4 weeks and then killed. Superoxide dismutases were detected by specific RIAs: catalase by polarography, and lipid peroxide by fluorimetry. Hypothyroid rats failed to grow, while hyperthyroid rats had hypertrophied hearts but no growth failure. An increase in lipid peroxide was observed in the soleus and heart muscles of hyperthyroid rats. This was accompanied by an increase in mitochondrial superoxide dismutase and oxidative markers. No such change was observed in either fast glycolytic muscle or liver. Glutathione peroxidase decreased in all tissues of hyperthyroid rats, and there was a parallel decrease in catalase in most tissues. On the other hand, hypothyroidism induced a reduction in oxidative markers and mitochondrial superoxide dismutase in heart and skeletal muscles, but only a marginal change in lipid peroxidation. The cytosolic superoxide dismutase did not change in relation to either oxidative metabolism or lipid peroxidation. These results suggest that the enhanced oxidative metabolism and decreased glutathione peroxidase in hyperthyroidism result in an increase in lipid peroxidation and, in slow oxidative and heart muscle, possible organ damage. No adverse reaction mediated by active oxygen species was found in hypothyroid rat tissues.

Animals↗
PubMed1990

Alterations of human growth hormone binding by rat liver membranes during hypo- and hyperthyroidism.

Hypothyroid rats treated with human GH (hGH) were partially refractory to the latter's effects. The present study was undertaken to investigate the role of hypo- and hyperthyroidism on the GH receptor. Seven-week-old rats were rendered either hypothyroid, by methimazole, or hyperthyroid, by a daily overdose of T4, during weeks 7-14 of life. Livers were homogenized and overlaid on sucrose discontinuous density gradient. Removal of endogenous ligand from the receptor was performed by exposing the membranes to MgCl2. hGH was used with excess ovine PRL to characterize somatogenic specific binding. Lactogenic specific binding was calculated by subtracting somatogenic specific binding from the total specific binding. Creatine kinase was also measured in homogenized livers. Liver membranes of the hypothyroid rats showed a significant decline in somatogenic and lactogenic binding of hGH. This was true for both the free unoccupied binding sites and total binding after dissociation of the endogenous ligand. Replacement of T4 for 2 weeks restored hGH binding to control values. Hyperthyroid rats had high somatogenic and lactogenic hGH binding. Creatine kinase activity decreased significantly in liver homogenates of hypothyroid rats, was restored by T4 replacement, and increased significantly in hyperthyroid rats. Thus, lactogenic and somatogenic receptors are directly related to the thyroid status in vivo.

Animals↗
PubMed2005

Reversible diastolic dysfunction after long-term exogenous subclinical hyperthyroidism: a randomized, placebo-controlled study.

BACKGROUND: Subclinical hyperthyroidism has been reported to affect systolic and diastolic cardiac function. However, the reversibility of these effects is not well established. OBJECTIVE: Our objective was to investigate the presence and reversibility of cardiac abnormalities in patients with long-term exogenous subclinical hyperthyroidism. DESIGN: We conducted a prospective, single-blinded, placebo-controlled randomized trial of 6 months duration with two parallel groups. SETTING: The study occurred at the Leiden University Medical Center, a tertiary referral center for thyroid carcinoma. PATIENTS: As a model for subclinical hyperthyroidism, 25 patients with a history of differentiated thyroid carcinoma with more than 10 yr of TSH suppressive therapy with L-T4 were studied. INTERVENTIONS: L-T4 dose was replaced by study medication containing L-T4 or placebo. Medication was titrated in a single-blinded fashion to establish continuation of TSH suppression (low-TSH group) or euthyroidism (euthyroid group). MEASUREMENTS: We assessed serum levels of free T4 and TSH and used echo Doppler cardiography including tissue Doppler to establish left ventricular (LV) dimensions and function as well as diastolic function. Baseline echocardiography data were compared with 24 controls. RESULTS: There were no differences in baseline cardiac parameters and TSH levels between the two groups. Although mean LV mass index was increased as compared with 24 controls, only four patients had LV hypertrophy at baseline. This was not improved by restoration of euthyroidism. At baseline, diastolic function was impaired in all patients as indicated by abnormal values for the peak flow of the early filling phase (E, 55.3 +/- 9.5 mm/sec), the ratio of E and the peak flow of the atrial filling phase (E/A ratio, 0.87 +/- 0.13), the early diastolic velocity obtained by tissue Doppler (E', 5.7 +/- 1.3 cm/sec), and the peak atrial filling velocity obtained by tissue Doppler (A', 6.8 +/- 1.4 cm/sec), prolonged E deceleration time (234 +/- 34 msec), and isovolumetric relaxation time (121 +/- 15 msec). After 6 months, significant improvements were observed in the euthyroid group in the E/A ratio (+41%; P < 0.001), E deceleration time (-18%; P = 0.006), isovolumetric relaxation time (-25%; P < 0.001), E' (+31%; P < 0.001), and the E'/A' ratio (+40%; P < 0.001). CONCLUSIONS: We conclude that prolonged subclinical hyperthyroidism is accompanied by diastolic dysfunction that is at least partly reversible after restoration of euthyroidism. Because isolated diastolic dysfunction may be associated with increased mortality, this finding is of clinical significance.

Adult↗
PubMed2005

Multicenter study on the prevalence of sexual symptoms in male hypo- and hyperthyroid patients.

CONTEXT: Thyroid hormones have a dramatic effect on human behavior. However, their role on sexual behavior and performance has seldom been investigated in men. OBJECTIVE: The objective of this study was to evaluate the prevalence of sexual dysfunctions in patients with hyper- and hypothyroidism and their resolution after normalization of thyroid hormone levels. DESIGN AND SETTING: We conducted a multicenter prospective study at endocrinology and andrology clinics in university hospitals. PATIENTS: The study included 48 adult men, 34 with hyperthyroidism and 14 with hypothyroidism. MAIN OUTCOME MEASURES: Subjects were screened for hypoactive sexual desire (HSD), erectile dysfunction (ED), premature ejaculation (PE), and delayed ejaculation (DE) on presentation and 8-16 wk after recovery from the thyroid hormone disorder. RESULTS: In hyperthyroid men, HSD, DE, PE, and ED prevalence was 17.6, 2.9, 50, and 14.7%, whereas in hypothyroid men, the prevalence of HSD, DE, and ED was 64.3% and of PE was 7.1%. After thyroid hormone normalization in hyperthyroid subjects, PE prevalence fell from 50 to 15%, whereas DE was improved in half of the treated hypothyroid men. Significant changes were found in the subdomains of the International Index of Erectile Function; ejaculation latency time doubled after treatment of hyperthyroidism (from 2.4 +/- 2.1 to 4.0 +/- 2.0 min), whereas for hypothyroid men it declined significantly, from 21.8 +/- 10.9 to 7.4 +/- 7.2 (P < 0.01 for both). TSH and thyroid hormone levels normalized rapidly after treatment, and changes in circulating sex steroids partially reflected the changes in SHBG levels. CONCLUSIONS: In summary, most patients with thyroid hormone disorders experience some sexual dysfunctions, which can be reversed by normalizing thyroid hormone levels. Despite the associated changes in sex hormone levels, the high prevalence of ejaculatory disorders and their prompt reversibility suggest a direct involvement of thyroid hormones in the physiology of ejaculation.

Adrenergic beta-Antagonists↗
PubMed1976

Recurrent hyperthyroidism in an acromegalic patient previously treated with proton beam irradiation: Graves' disease as probable etiology based on follow-up observations.

A 56-year-old woman presented in 1973 with hyperthyroidism and partial anterior pituitary insufficiency. Three years before she had undergone pituitary irradiation for acromegaly and hyperthyroidism, the latter was attributed at the time to excessive TSH secretion because of elevations in plasma TSH. During the present 11/2 years of observation, TSH levels were appropriately low and did not respond to iv TRH when the patient was hyperthyroid. Moreover, they did not rise during treatment, even as the patient became borderline hypothyroid. It is concluded that hyperthyroidism probably has always been due to Graves' disease.

Acromegaly↗
PubMed1976

Hyperthyroidism with normal concentrations of total serum thyroxine and triiodothyronine.

Normal concentrations of total serum thyroxine (T4) and triiodothyronine (T3) were found in a patient who was hyperthyroid because of a hyperfunctioning thyroid adenoma. After surgical removal of the adenoma, the patient became clinically euthyroid; the abnormally high free thyroxine (FT4), triiodothyronine resin uptake (T3R) and rapid achilles reflex time (ART) returned to normal. A low-normal concentration of thyroxine binding globulin (TBG) determined by polyacrylamide gel electrophoresis and a low level of TBG determined by radioimmunoassay were found in the patient. The TBG remained low-normal after the restitution of euthroidism. Low TBG levels were found in the patients 5 brothers and maternal uncle, and a low-normal concentration was found in her mother. It is postulated that the patient was heterozygous carrier for a genetically determined partial (non-zero) TBG deficiency and that a low-normal TBG concentration decreased total T3 as well as T4 when the patient was hyperthyroid. To the author's knowledge, this is the first case of hyperthyroidism associated with both normal total T4 and T3 concentrations. The diagnosis of hyperthyroidism in the presence of low TBG is difficult, and determination of FT4 and free triiodothyronine (FT3) may be necessary to establish the diagnosis.

Adenoma↗
PubMed1977

Catecholamine metabolism in thyroid disease. II. Norepinephrine secretion rate in hyperthyroidism and hypothyroidism.

We have measured the secretion rate of norepinephrine (NE) in 6 euthyroid subjects, 6 hyperthyroid and 6 hypothyroid patients, infused at a constant rate (0.1 microC/kg/min) for 1 h with tritiated norepinephrine (New England Nuclear Inc.). Plasma NE concentrations were measured by a modification of the fluorometric method of Anton and Sayre. A significant linear relationship was observed between plasma NE and age in normal subjects. Accordingly, values for plasma NE have been corrected for age. Plasma NE concentration was 18.3 +/- 4.2 ng/100 ml (mean+/-SEM) in normal subjects compared with 17.5 +/- 3.3 ng/100 ml in hyperthyroid patients. There was a significant elevation of plasma NE (30.3 +/- 2.9 ng/100 ml) in hypothyroid patients (P less than 0.05). A significant elevation was observed in plasma NE secretion rates in hypothyroidism 4.62 +/- 0.98 microgram/kg/day (P less than 0.02) when compared to the control group (1.46 +/- 0.35 microgram/kg/day). No significant difference was observed between the hyperthyroid group (1.74 +/- 0.49 microgram/kg/day) and the controls. These data indicate that the plasma NE secretion rate is normal in hyperthyroidism, and is significantly elevated in hypothyroidism thereby explaining the higher plasma NE concentrations seen in hypothyroidism.

Epinephrine↗
PubMed1978

Evaluation of triiodothyronine (T3) kinetics in normal subjects, in hypothyroid, and hyperthyroid patients using specific antiserum for the determination of labeled T3 in plasma.

Triiodothyronine (T3) kinetics was evaluated using [125I]T3 and the single injection technique; 5 hypothyroid, 6 hyperthyroid patients, and 10 euthyroid control subjects were studied. Plasma-labeled T3 concentration was measured by means of a new method based on extraction of the hormone on Sephadex G-25 columns followed by elution with the specific antiserum. This technique allows a far better separation of the hormonal radioactivity from the labeled iodide produced from T3 catabolism in comparison with the TCA-precipitation-butanol extraction method. The analysis of the experimental data has been performed using non-compartmental treatment (integral approach); results of mono-compartmental analysis of the same data are also reported for comparison. Average metabolic clearance was 15.3 +/- 0.6 (mean + SEM) liters/day/m2 body surface in normal subjects; it was significantly decreased in hypothyroid patients (11.4 +/- 1.1) and significantly increased (33.4 +/- 4.0) in hyperthyroidism. The total plasma equivalent distribution volume was found significantly enlarged in hyperthyroid patients (22.6 +/- 0.9 liters/m2) in respect to that measured in the control group (15.6 +/- 0.4), whereas it was not different from normal value in hypothyroid patients (17 +/- 1.7). Using plasma concentration of native T3, absolute turnover rate and extrathyroidal pool were also estimated; their values were 6.5, 23.7, and 131.7 micrograms/day/m2 and 10.1, 24.2, and 90.6 micrograms/m2, respectively, in hypothyroid, normal, and hyperthyroid groups.

Adolescent↗
PubMed1979

Regulation of lipolysis by human adipose tissue in hyperthyroidism.

The effects of noradrenaline (NA) and isopropyl-noradrenaline (ISNA) on glycerol release and cAMP levels in sc adipose tissue were studied in vitro in 27 patients with hyperthyroidism. In 11 patients, the studies were repeated after 6--12 months of treatment for hyperthyroidism. A third group comprised 21 euthyroid patients otherwise healthy except for morbid obesity. The lipolytic response to ISNA, observed in untreated thyrotoxic patients, was found to be reduced by 30% when the patients were reexamined after treatment for thyrotoxicosis. This reduction was attributable to a decrease in the cAMP level. This was observed whether adipose tissue was incubated in the presence or absence of a phosphodiesterase inhibitor, theophylline. Both NA and ISNA induced 50% more rapid glycerol release and 4 times higher cAMP levels in adipose tissue of the thyrotoxic subjects than in the obese euthyroid patients. A positive correlation between tissue cAMP and glycerol release, on one hand, and mean fat cell size, on the other hand, was observed in treated thyrotoxic patients and obese euthyroid patients but was not recorded in the untreated hyperthyroid patients. The basal rate of lipolysis was not altered in thyrotoxicosis. The results suggest that the enhanced lipolytic response to catecholamines in adipose tissue of hyperthyroid patients is due to increased beta-adrenergic responsiveness. In addition, a disruption in subsequent stages of the regulatory pathway at the level of protein kinase or hormone-sensitive lipase also seems possible.

Adipose Tissue↗
PubMed1979

Lack of evidence for thyrotropin-releasing hormone deamidation in normal and hyperthyroid human sera.

Two-hour incubations of human serum with 50 ng TRH or pyroglutamyl-histidyl-proline (TRH-OH) were performed under substrate conditions of 0.2 microgram substrate/ml serum. During incubations with normal serum, 46.3 +/- 1.3 (SEM) ng TRH were degraded while only 14.2 +/- 5.1 ng TRH-OH were degraded (P less than 0.001). During incubations with serum from patients with hyperthyroidism, 42.7 +/- 2.6 ng TRH were degraded compared to only 19.6 +/- 2.0 ng TRH-OH (P less than 0.001). Despite the fact that TRH degradation was significantly greater than TRH-OH degradation in both normal and hyperthyroid serum, no formation of TRH-OH (less than 3.1 ng/incubation tube) from TRH was detected. Formation of TRH-OH from TRH was also not noted when normal or hyperthyroid serum was incubated with TRH at substrate concentrations of 62.5 microgram/ml serum. These data confirm other reports that TRH deamidation does not occur in normal serum and extends this observation to hyperthyroid serum.

Humans↗
PubMed1981

Changes in the effects of insulin on human adipose tissue metabolism in hyperthyroidism.

The in vitro effects of insulin on glycerol release and glucose incorporation into neutral lipids (lipogenesis) were studied in segments of sc adipose tissue obtained from 9 control subjects and 11 patients with hyperthyroidism; 6 patients were reinvestigated after treatment. In untreated hyperthyroidism, there was a decreased sensitivity to the antilipolytic effect of insulin, since the dose-response curve was shifted to the right; 250 microU/ml insulin were required for 50% of the maximal effect compared to 25 microU/ml in the controls. During antithyroid therapy, the dose-response curve normalized. Insulin caused a 25% increase in lipogenesis in the untreated hyperthyroid patients, but no consistent effect was seen in the control subject or in hyperthyroid patients during treatment.

Adipose Tissue↗
PubMed1982

Prolactin response to metoclopramide in hyperthyroidism.

The response of PRL to the oral administration of the dopamine receptor-blocking agent metoclopramide and the effect of metoclopramide on the TRH-induced release of PRL and TSH were measured in eight patients with hyperthyroidism and in eight age- and sex-matched euthyroid controls. As expected from the known direct inhibitory influence of thyroid hormones on pituitary TSH secretion, there was no TSH rise in response to metoclopramide in either group. PRL levels, on the other hand, rose significantly after the administration of metoclopramide in both the hyperthyroid and euthyroid subjects (P less than 0.0005 at 60 and 120 min). However, the increase in PRL at 120 min was significantly less in the hyperthyroid subjects than in the euthyroid controls (P less than 0.0025). Furthermore, the administration of metoclopramide failed to reestablish normal responsiveness of either PRL or TSH to TRH in the hyperthyroid subjects. We have previously suggested that thyroid hormones inhibit PRL secretion by stimulating the hypothalamic secretion of dopamine. These results suggest, however, that elevated levels of thyroid hormones also inhibit PRL release directly at the anterior pituitary level.

Administration, Oral↗
PubMed1982

Simultaneous measurement of 3,5-diiodothyronine and 3,5,3'-triiodothyronine turnover kinetics in euthyroid hyperthyroid, and hypothyroid subjects.

Simultaneous kinetic studies of 3,5-diiodothyronine (3,5-T2) and T3 were performed in 15 healthy controls (8 men and 7 women), 7 hyperthyroid patients (2 men and 5 women), and 6 hypothyroid women using the single injection, noncompartmental approach. The serum concentrations (picomoles per liter), MCRs (liters . day-1 . (70 kg)-1), and production rates (PRs; nmol . day-1 . (70 kg)-1) of 3,5-T2 in healthy men and women were (mean +/- SD): 100 +/- 23 vs. 80 +/- 23 (P = NS), 59 +/- 31 vs. 123 +/- 58 (P less than 0.025), and 5.6 +/- 1.9 vs. 9.1 +/- 2.6 (P less than 0.02). The conversion rate (CR) of T3 to 3,5-T2 was 12.0 +/- 3.8% in men compared to 18.5 +/- 3.7% in women (P less than 0.01). Serum 3,5-T2 levels in five mildly hyperthyroid women were elevated to 123 +/- 33 pmol/liter (P less than 0.05), whereas the MCR and PR were unchanged. However, two hyperthyroid men with more pronounced elevation of serum T3 had enhanced PRs (26.9 and 23.9 nmol . day-1 . (70 kg)-1). The CR in hyperthyroid women was significantly reduced to 5.6 +/- 2.9% (P less than 0.001). The serum levels, MCR, and PR of 3,5-T2 in hypothyroid women were: 58 +/- 25 pmol/liter (P = NS), 71 +/- 52 liters . day-1 . (70 kg)-1 (P = NS), and 3.4 +/- 2.4 nmol . day-1 . (70 kg)-1 (P less than 0.005). The CR was enhanced to 34.8 +/- 15.7% (P less than 0.05). Our data demonstrate that in euthyroid subjects, approximately 15% of T3 is deiodinated to 3,5-T2, and this 5'-deiodination of T3 is influenced by thyroid function.

Adult↗
PubMed1982

Serum lipids and apolipoproteins A-I, A-II, and B in hyperthyroidism before and after treatment.

The serum concentrations of total cholesterol (TC), triglycerides (RG), high density lipoprotein-cholesterol (HDLc), low density lipoprotein-cholesterol (LDLc), and the apolipoproteins (apo) A-I, A-II, and B were measured in 33 hyperthyroid patients before and after treatment. The results were compared with those of healthy controls. Apo A-I, A-II, and B were assayed by immunonephelometry. The serum levels of TC (mean +/- SD, 167 +/- 36 mg/dl, HDLc (40.8 +/- 12 mg/dl), and LDLc (108 +/- 35 mg/dl) were decreased in the untreated hyperthyroid patients compared to both the values after treatment (TC: 215 +/- 54 mg/dl; P less than 0.001; HDLc: 52 +/- 14 mg/dl; P less than 0.001; LDLc: 146 +/- 47 mg/dl; P less than 0.001) and the control values (TC: 206 + 39 mg/dl; P less than 0.001; HDLc: 47.4 +/- 10 mg/dl; P les than 0.01; LDLc: 145 +/- 38 mg/dl; P less than 0.001). TG levels were not statistically different before and after treatment. The apo A-I concentrations (116 +/- 24 mg/dl) were lower before than after treatment (131 +/- 28 mg/dl; P less than 0.01), but they were not statistically different from those in the control group (115 +/- 19 mg/dl). The apo A-II levels were identical in all groups (before treatment, 35 +/- 7 mg/dl; after treatment, 37 +/- 9 mg/dl; control group, 36 +/- 9 mg/dl). The apo B levels were lower in the untreated hyperthyroid patients (86 +/- 23 mg/dl) compared to those in controls (103 +/- 19 mg/dl; P less than 0.001) and patients after therapy (103 +/- 25 mg/dl; P less than 0.001). The increase in HDLc relative to the major HDL apo A-I and A-II during treatment for hyperthyroidism was associated with changes in body weight. The apo A-I to apo A-II and LDLc to apo B ratios, however, were significantly lower before compared to those after treatment, when the influence of increasing body weight during therapy was accounted for. This study emphasizes the important regulating role of thyroid hormones on lipid and apolipoprotein metabolism.

Apolipoprotein A-I↗
PubMed1983

Pregnancy-associated changes in the thyroid-stimulating antibody of Graves' disease and the relationship to neonatal hyperthyroidism.

Assays for the thyroid-stimulating antibody (TSAb) of Graves' disease were performed with serum obtained from 17 women with 20 pregnancies who either had or had had Graves' disease, or who had delivered a child with neonatal hyperthyroidism. Ten of the children, of eight women, were diagnosed as being hyperthyroid; all eight mothers had high concentrations of TSAb, as measured by adenylate cyclase stimulation. In the infants with neonatal hyperthyroidism, a minimum 500% increase in cAMP was found on assay of maternal immunoglobulin G, and no such high values were associated with a euthyroid infant. Blood samples for TSAb assay were available from 11 mothers on both the day of delivery and at least 1 other time in the pre- or postpartum period. In 7 mothers, the lowest value (negative in 4) was obtained coincident with delivery, and in the remaining 4, there was no pregnancy-associated change. Thus, a pattern, related to pregnancy, of a decline in TSAb concentration or a subsequent postpartum increase was observed in the majority of subjects. Apparently, neonatal hyperthyroidism due to transplacental passage of TSAb occurred only when this decline did not reduce the concentration to a low value.

Antibodies↗
PubMed1983

Glucagon binding autoantibodies in a patient with hyperthyroidism treated with methimazole.

A 47-yr-old woman who had previously received methimazole (MMI) treatment for hyperthyroidism was found to have glucagon binding autoantibodies in plasma. She had never received glucagon. The binding substances were detected in plasma at the time of a glucagon RIA. [125I]Glucagon binding was inhibited only by porcine glucagon and porcine glicentin, and dissociated at acid pH. The substances proved to be glucagon binding antibodies (immunoglobulin G, L-chain K-type), as determined by ammonium sulfate and radioprecipitation. There were no clinical manifestations related the presence of these autoantibodies. In a survey of 91 patients with thyroid disease, 3 patients whose plasma bound [125I]glucagon were identified among 41 with hyperthyroidism who were receiving MMI treatment. Such binding was not found in plasma from untreated hyperthyroid patients, those receiving propylthiouracil or those with chronic thyroiditis. These findings suggest that the development of glucagon antibodies in hyperthyroidism may be associated with MMI treatment.

Autoantibodies↗
PubMed1984

Splanchnic extraction of 3,3'-diiodothyronine and 3',5'-diiodothyronine in hyperthyroidism.

The splanchnic extraction of 3,3'-diiodothyronine (3,3'-T2) and 3',5'-diiodothyronine (3',5'-T2) was studied in 7 hyperthyroid patients and 20 normal subjects employing the hepatic venous catheterization technique. A significant net uptake by splanchnic tissues was found for both diiodothyronines . The fractional splanchnic extraction calculated as the arterio-hepatic venous plasma concentration difference divided by the arterial concentration was unaffected by hyperthyroidism as compared to normal values. There was a close positive correlation between the arterio-hepatic venous concentration difference and arterial concentration, 3,3'-T2: r = 0.988, and 3',5'-T2: r = 0.932 (P less than 0.001). The splanchnic extraction was nonsaturable at endogenous plasma concentrations of 3,3'-T2 up to at least 17.0 ng/dl and of 3',5'-T2 up to at least 15.2 ng/dl. The data suggest that the splanchnic extraction of 3,3'-T2 and 3',5'-T2 obeys first order kinetics, the fractional extraction being unaffected by hyperthyroidism. Furthermore, changes in the net splanchnic extraction of 3,3'-T2 and 3',5'-T2 do not seem to contribute to changes in circulating levels of these iodothyronines. It is suggested that tissues other than the liver contribute significantly to the deiodination process both in normal and in hyperthyroid man.

Adolescent↗
PubMed1985

Glucose metabolism in noninsulin-dependent diabetic patients with experimental hyperthyroidism.

Hyperthyroidism is known to further impair carbohydrate metabolism in diabetic patients. In the present study we examined in noninsulin-dependent (type 2) diabetic patients the effect of T3-induced hyperthyroidism on glucose utilization and endogenous glucose production by means of the hyperinsulinemic and hyperglycemic clamp technique in combination with [3H]3-glucose kinetic analysis. Administration of T3 for 1 week increased the mean serum T3 concentration from 1.0 +/- 0.1 (SEM) to 4.1 +/- 0.2 ng/ml, and the mean fasting plasma glucose from 8.7 +/- 0.7 to 9.9 +/- 0.9 mmol/liter. Basal hepatic glucose production (HGP) rose from 3.23 +/- 0.23 to 3.98 +/- 0.25 mg/kg X min, whereas basal MCR of glucose (MCRG) increased only slightly from 2.12 +/- 0.24 to 2.30 +/- 0.14 ml/kg X min. When the plasma insulin concentration was acutely raised and maintained at 82 +/- 8 microU/ml (hyperinsulinemic clamp study), HGP decreased to 0.71 +/- 0.29 mg/kg X min and MCRG increased to 3.16 +/- 0.47 ml/kg X min. After T3 administration suppression of HGP by insulin was reduced (1.55 +/- 0.37 mg/kg X min), but at the same time MCRG was only slightly affected (3.64 +/- 0.54 ml/kg X min). In the hyperglycemic clamp study the plasma glucose concentration was maintained 7 mmol/liter above the individual fasting level. MCRG was again slightly higher after T3 administration (1.98 +/- 0.18 vs. 1.66 +/- 0.15 ml/kg X min), but insufficient to completely compensate for the higher residual HGP at the hyperthyroid as compared to the euthyroid state (2.42 +/- 0.24 vs. 1.45 +/- 0.36 mg/kg X min). Thus, deterioration of metabolic control in noninsulin-dependent diabetic patients by hyperthyroidism is due primarily to enhancement of basal HGP and its reduced suppressibility by insulin and glucose.

Adult↗