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PubMed1985

[Insulin, glucagon and growth hormone responses during glucose, arginine and insulin tolerance tests in children with hyperthyroidism].

There are many reports of glucose intolerance in adult patients with hyperthyroidism but few reports of glucose intolerance in hyperthyroid children. In this study, we measured plasma levels of glucose, insulin, glucagon and growth hormone in hyperthyroid children and control subjects by the use of three kinds of tolerance tests: an oral glucose tolerance test, an arginine tolerance test and an insulin tolerance test. In the oral glucose tolerance test, mean fasting glucose levels (79.6 +/- 1.4 mg/dl) rose to maximum levels (157.3 +/- 4.3 mg/dl) at 30 min in hyperthyroid children which were significantly higher than the levels in control subjects (p less than 0.01). The maximum levels of glucose fell slowly and returned to fasting levels at 180 min. In this test, plasma insulin levels increased from basal levels (12.7 +/- 1.9 microU/ml) to maximum levels (120.8 +/- 22.1 microU/ml) at 30 min in the prepubertal age group of hyperthyroidism. On the other hand, in the pubertal age group of hyperthyroidism, maximum levels of insulin were observed at 60 min, but not at 30 min. These maximum levels of insulin of both hyperthyroid age groups were significantly higher than those in the control subjects (p less than 0.05, p less than 0.01 respectively). There was no difference in insulin-glucose ratio at 30 min (delta IRI/delta BG) and insulinogenic index (I.I.) at 0 to 60 min between these two groups of hyperthyroid children and control subjects. However, I.I. at 0 to 120 min and 0 to 180 min decreased significantly in the pubertal age group of hyperthyroidism as compared with those in the control group (p less than 0.05, p less than 0.02 respectively). In the oral glucose tolerance test, plasma glucagon levels decreased from basal levels (74.1 +/- 4.3 pg/ml) to minimum levels (36.4 +/- 4.7 pg/ml) at 90 min in hyperthyroidism, which were significantly lower than those in the controls (p less than 0.05). However, there was no difference in -epsilon delta IRG/epsilon delta BG (cumulative glucagon response/cumulative glucose response) between the subjects with hyperthyroidism and the controls. On the other hand, lower responses of blood glucose, insulin, glucagon and growth hormone to arginine were observed in subjects with hyperthyroidism than in the controls. Moreover in the insulin tolerance test, there was no difference in glucagon and growth hormone response between the subjects with hyperthyroidism and the controls. Thus our conclusions are as follows: A marked increase in blood glucose after oral glucose load was observed in spite of normal insulin-glucose ratio in hyperthyroid children, suggesting the existence of peripheral insulin resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1989

Significance of latent hyperthyroidism.

In euthyroidism the circadian rhythm and pulsatility of TSH is well known. With regard to hyperthyroidism only very preliminary data were described. In this study we investigated the secretion pattern of the pituitary-thyroid axis hormones during 24 h in latent and overt hyperthyroidism and in euthyroidism with regard to common and different properties. Blood was obtained for 24 h at 10-min intervals. In euthyroidism we found intraindividually three overlapping patterns of TSH, which are different in amplitude and frequency and can be found interindividually, too. These patterns are equal to the circadian rhythm, pulsatile secretion and lastly to the methodic rustle. The circadian rhythm in latent hyperthyroidism is distinctly suppressed and in overt hyperthyroidism totally. Whereas in latent hyperthyroidism pulsatile secretion is extant, in overt hyperthyroidism the TSH pulses are absent. To record the patients' TSH circadian rhythm with only three blood samples, we defined the TSH-Triplex. In young as well as in elderly healthy volunteers it demonstrated significantly higher TSH levels at midnight (at 24:00 h) than it did at 4 p.m. and 8 a.m. The present study shows a significantly different TSH pattern in latent hyperthyroidism compared to euthyroidism. It should be discussed whether latent hyperthyroidism could be defined as hyperthyroidism stage I. On the other hand, latent hyperthyroidism could be an illness with its own cause, different from hyperthyroidism. Our data suggest that the laboratory findings of latent hyperthyroidism in each age are non-physiological. However, the cause for this disorder is unclear until now; hence further investigations are necessary.

Adult↗
PubMed1992

Hyperthyroidism selectively modified a transient potassium current in rabbit ventricular and atrial myocytes.

1. Transient outward potassium currents (I(t)) were compared in single cardiac myocytes obtained from normal and hyperthyroid rabbits. Currents were recorded using the suction electrode whole-cell voltage clamp technique. 2. In ventricular myocytes from hyperthyroid animals (at 22 degrees C and a stimulation rate of 0.2 Hz), I(t) was 4- to 5-fold larger than in normal myocytes, in a potential range of -20 to +60 mV. As in normal myocytes, I(t) in hyperthyroid myocytes was calcium insensitive, and was more than 90% suppressed by 2 mM 4-aminopyridine. 3. The increase in I(t) was observed over a wide range of stimulation rates, even at rates sufficiently slow to enable complete reactivation of the I(t) channels. However, there was a major change in the rate dependence of I(t) in hyperthyroid myocytes, with significant I(t) current still present at rates (e.g. 1-2 Hz) at which it is normally completely suppressed. 4. The augmentation of I(t) in the hyperthyroid myocytes could not be accounted for by changes in the voltage dependence or the kinetics of channel activation or inactivation. There was no change in the reversal potential of I(t), implying no change in the selectivity of the channel. 5. Single-channel activity was recorded using the cell-attached mode of recording. In myocytes from hyperthyroid rabbit we observed the following: (a) active patches (often containing two channels) were obtained more frequently in comparison to control; (b) the unitary conductance of the channel was the same; (c) single-channel openings persisted at high stimulation rates. 6. In contrast to hyperthyroid ventricular cells, I(t) in atrial cells from the same hearts was not substantially changed. 7. The rate dependence of I(t) in atrial cells was also unaffected by hyperthyroidism, in contrast to the large changes observed in ventricular cells. Thus, in atrial cells from hyperthyroid hearts the current was totally suppressed at rates of 1-2 Hz, as in euthyroid conditions. 8. Single-channel recordings in the cell-attached mode showed a unitary conductance similar to that found in normal atrial cells. Channel activity was suppressed at 2 Hz, in contrast to hyperthyroid ventricular cells. 9. In conclusion, I(t) is drastically changed in hyperthyroid rabbit ventricle cells. The changes are in the magnitude of the macroscopic current and its rate dependence. Since the unitary conductance is unchanged (and the peak open probabilities are normally high at positive membrane potential(s) the number of active channels in the membrane must be increased. In atrial cells from the same hyperthyroid hearts no changes are apparent.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1991

Species differences in myocardial beta-adrenergic receptor regulation in response to hyperthyroidism.

The coupling between myocardial beta-adrenergic receptors, adenylate cyclase activity, and the in vivo cardiac response to catecholamines is controversial in hyperthyroidism. The possibility of species differences in beta-adrenoceptor regulation after thyroxine treatment was studied in dogs and in rats. In dogs instrumented with a left ventricular (LV) pressure micromanometer, hyperthyroidism was induced by L-thyroxine (0.5 mg/kg/day i.v. for 10 days). After hyperthyroidism, heart rate was increased to 167 +/- 10 beats/min (control, 107 +/- 8 beats/min; p less than 0.005) with an increase of peak LV dP/dt from 4,243 +/- 471 to 6,105 +/- 862 mm Hg/sec (p less than 0.01). LV response to injection of increasing doses of isoproterenol and dobutamine was not significantly different before and after induction of the hyperthyroid state, as shown by the unchanged slopes of the LV peak dP/dt versus the log of the dose of isoproterenol and dobutamine. Bmax of beta-receptors measured in crude membranes using 3H-CGP 12177 and in homogenates using 125I-cyanopindolol was not increased in hyperthyroid animals as compared with a control group. Basal adenylate cyclase activity was not different in control and hyperthyroid dogs (32 +/- 3 versus 29 +/- 3 pmol/mg/min), and maximal adenylate cyclase activity response to isoproterenol was similar in control and hyperthyroid dogs. In contrast, in rats subjected to hyperthyroidism (0.5 mg/kg/day i.p. L-thyroxine for 10 days), Bmax of adrenoceptors measured using the same methods was significantly increased as compared with control (+72.5% using 3H-CGP 12177 and +41% using 125I-cyanopindolol, but adenylate cyclase activity was not increased in hyperthyroid rats. We conclude that both adenylate cyclase activity and LV response to catecholamines are not increased by thyroxine-induced hyperthyroidism in dogs and that, in contrast with rats, beta-adrenergic density is not increased in hyperthyroid dogs. This indicates a species difference in myocardial beta-adrenoceptor regulation in response to hyperthyroidism.

Adenylyl Cyclases↗
PubMed1980

Enhanced contractile response and protein kinase activation to threshold levels of beta-adrenergic stimulation in hyperthyroid rat heart.

The contractile response measured as maximum rate of force development to a near threshold concentration of isoproterenol (1 nM) was enhanced in perfused interventricular septa from hyperthyroid (128+/-4% control) compared with euthyroid rats (105+/-2%, P < 0.01). This enhanced contractile response was accompanied by a significant activation of cyclic (c)AMP-dependent protein kinase (protein kinase activity ratio increased from 0.159+/-0.008 to 0.218+/-0.019, P < 0.005, although no significant changes from base line occurred in euthyroid septa, 0.152+/-0.007-0.179+/-0.012). No difference between hyperthyroid and euthyroid hearts was observed in the contractile response to 0.1 mM dibutyryl cAMP (126.5+/-2.5% and 122.0+/-9.2% in hyperthyroid and euthyroid, respectively), and the magnitude of the response to dibutyryl cAMP was comparable with that observed in the hyperthyroid group with 1 nM isoproterenol. These results suggest that the mechanism for enhanced protein kinase activation and contractile response to low concentrations of isoproterenol in the hyperthyroid heart is at or proximal to cAMP generation. The maximum contractile response to isoproterenol (0.5 muM), however, was decreased in hyperthyroid myocardium (192+/-13%) compared with euthyroid (291+/-37%, P < 0.05). Both protein kinase activity ratio (0.356+/-0.017 and 0.344+/-0.013) and the maximum contractile response to Ca(++) (335+/-15 and 340+/-12% control in hyperthyroid and euthyroid, respectively) were similar, suggesting that the mechanism of the diminished maximum response was distal to protein kinase activation but not a function of an altered Ca(++)-troponin interaction. The diminished maximum rate of force development response in the hyperthyroid hearts was accompanied by significantly less shortening of the contraction duration that was 85.6+/-2.1% control in hyperthyroid vs. 66+/-2.8% control in euthyroid, P < 0.001. Although the basal rate of Ca(++) accumulation was greater in microsomes isolated from hyperthyroid than from euthyroid hearts, there was significantly less additional stimulation of Ca(++) accumulation in response to exogenous cAMP and protein kinase in hyperthyroid compared with euthyroid hearts. This reduction may explain the diminished effect of isoproterenol on the shortening of contraction duration in hyperthyroid compared with the euthyroid myocardium, and may explain, at least in part, the diminished maximum contractile response to isoproterenol.

Adrenergic beta-Agonists↗
PubMed1980

Impaired pancreatic alpha-cell response in hyperthyroidism.

Recently, we observed that in hyperthyroid patients, plasma glucagon was not adequately suppressed by an oral glucose load, suggesting altered pancreatic alpha-cell sensitivity. To further assess pancreatic alpha-cell function in hyperthyroidism, plasma glucose, glucagon, and insulin resonses to a protein meal were determined in normal subjects and hyperthyroid patients. Fasting plasma glucose was normal in hyperthyroid patients. A protein meal produced an increase in plasma glucose levels in hyperthyroid patients, whereas in normal subjects protein feeding was followed by a decline in blood glucose levels. Basal glucagon was markedly elevated in three of nine hyperthyroid patients, whereas in the remaining six, fasting plasma glucagon was unaltered. In both groups, protein feeding induced a glucagon rise; however, the increment was significantly smaller in hyperthyroid patients. In hyperthyroidism, fasting plasma insulin was raised and the insulin response to a protein meal was exaggerated. Furthermore, the insulin elevations were sustained and did not return to the basal level by 180 min as observed in normal subjects. We conclude that 1) the plasma glucagon response to a protein meal is blunted in hyperthyroidism, a finding which confirms our recent observation of decreased sensitivity of the pancreatic alpha-cell in hyperthyroidism; 2) fasting hyperinsulinemia with simultaneous euglycemia is consistent with the presence of insulin resistance in hyperthyroidism; and 3) the sustained and exaggerated plasma insulin rise after ingestion of a protein meal suggests hypersensitivity of the pancreatic beta-cell in hyperthyroidism.

Adolescent↗
PubMedDate not supplied

Enhanced myocardial contractility but not tachycardia persists in isolated working hyperthyroid rat hearts.

It is generally believed that the increased contractility and tachycardia of the hyperthyroid heart are a result of thyroid hormone-induced alterations of the mechanical and electrical properties of the heart, respectively. We compared the contractility (dP/dtmax) and the spontaneous beating rate of hyperthyroid and euthyroid hearts perfused in vitro in either a non-working or a working mode. The dP/dtmax (4196 +/- 74 mm Hg s-1) and beating rate (322 +/- 8 beats/min) of the non-working hyperthyroid hearts were significantly higher (p less than 0.001) than those of the euthyroid hearts (3267 +/- 115 mm Hg s-1 and 260 +/- 6 beats/min at an external Ca2+ of 2.5 mM). At 2.5 mM Ca2+, the working hyperthyroid hearts again displayed enhanced contractility (5636 +/- 179 mm Hg s-1 vs 4508 +/- 172 mm Hg s-1; p less than 0.001) but the spontaneous beating rate (275 +/- 7 beats/min) was not significantly different from euthyroid (261 +/- 8 beats/min). When hearts were subjected to periods of alternate non-working and working perfusion, the beating rate of the hyperthyroid hearts was significantly higher than euthyroid during non-working (p less than 0.02) but not during working perfusion. Increasing the afterload on the non-working preparations in a stepwise fashion from 75 cm H2O to 120 cm H2O caused significant changes in left ventricular pressure and dP/dtmax in both heart types but the tachycardia in the hyperthyroid hearts persisted (at 120 cm H2O; hyperthyroid, 294 +/- 9 beats/min; euthyroid, 224 +/- 10 beats/min; p less than 0.001). Alteration of the preload (10 to 25 cm H2O) and afterload (75 to 105 cm H2O) on working hyperthyroid and euthyroid hearts caused changes in both left ventricular pressure and dP/dtmax but the beating rates of both heart types were never significantly different. We conclude from our results that (i) the increased contractility of the hyperthyroid rat heart is due to thyroid hormone-induced alteration of the mechanical properties of the heart; (ii) the tachycardia of hyperthyroidism is not due to thyroid hormone-induced changes in the electrical properties of the heart, but probably involves some as yet unidentified chronotropic agent.

Animals↗
PubMed1995

Hyperthyroidism and seizures during pregnancy.

Untreated hyperthyroidism during pregnancy is associated with increased maternal and perinatal morbidity. Some features of this disease simulate preeclampsia, which may encourage delivery of the fetus. We report a case of poorly controlled hyperthyroidism associated with generalized seizures, where patient management was directed at a diagnosis of preeclampsia-eclampsia. Although the presence of eclampsia and marked hyperthyroidism is very rare, this case illustrates the importance of aggressive medical management of hyperthyroidism. A 17-year-old gravida was diagnosed with hyperthyroidism at 15 weeks' gestation. At 26 weeks' gestation, she was admitted to the hospital after noting edema of the upper and lower extremities, nausea, vomiting, shortness of breath, and a cough. At admission, she was hypertensive, tachycardic, and dyspneic. The patient was believed to have preeclampsia with pulmonary edema complicated by hyperthyroidism. We initiated magnesium sulfate therapy and administered several bolus doses of hydralazine, with little effect on blood pressure. Oliguria was noted, and a pulmonary artery catheter was inserted. Hours later, generalized seizure activity occurred, and a decision was made for abdominal delivery. Postoperatively, cardiovascular function stabilized. On postoperative day 3, we received the results of the thyroid function tests obtained at admission, which suggested a markedly hyperthyroid condition. Untreated or poorly treated hyperthyroidism may present a clinical picture similar to preeclampsia. In our case, both disease processes coexisted in their severest forms. It is possible, although completely unproven, that a relationship exists between poorly controlled hyperthyroidism and preeclampsia-eclampsia. More importantly, accurate diagnosis of hyperthyroidism should lead to prompt medical or surgical management, thereby decreasing maternal and perinatal morbidity.

Adolescent↗
PubMed1990

Modulation of stimulation frequency responses and calcium dependency of functional parameters in hyperthyroid rat ventricular papillary muscles.

The effects of stimulation frequency (0.2-1.5 Hz) and extracellular calcium concentration ([Ca2+]o) (0.6-15.0 mM) on the contractile function of thin papillary muscles of euthyroid and hyperthyroid rats were studied. Hyperthyroidism led to a decrease in developed tension (DT) and time to peak tension (TPT), but it exhibited no influence on the maximal rates of contraction (+dT/dt) and relaxation (-dT/dt). Also, the mean rates of contraction were similar in euthyroid and hyperthyroid muscle groups. The increase in stimulation frequency brought about a marked decrease in DT, +dT/dt, and -dT/dt of euthyroid papillary muscles at lower frequencies in comparison to papillary muscles in the hyperthyroid group. At stimulation frequencies above 1.0 Hz, the absolute and relative levels of DT and -dT/dt of hyperthyroid myocardium were elevated over euthyroid preparations. At the same time, TPT was unchanged in any of the muscle groups. Hyperthyroidism modulated the relationships between contractile parameters and [Ca2+]o. At a [Ca2+]o of 1.0-4.0 mM, the DT of hyperthyroid papillary muscles was lower than in euthyroid muscle. At 4.0 and 8.0 mM of [Ca2+]o, the equal values of maximal DT were registered for euthyroid and hyperthyroid papillary muscles, respectively. An increase in the [Ca2+]o in the range of 1.0-15.0 mM was accompanied by an increase in TPT of both muscle groups, but to a greater extent in hyperthyroid myocardium. In conclusion, the myocardium of hyperthyroid rat appeared to exhibit decreased sensitivity to calcium as well as to the negative inotropic effect of enhanced stimulation frequency. Alterations of the processes of transsarcolemmal movement and intracellular recycling of Ca2 may be implicated.

Animals↗
PubMed1988

Modulation of atrial natriuretic factor by thyroid hormone: messenger ribonucleic acid and peptide levels in hypothyroid, euthyroid, and hyperthyroid rat atria and ventricles.

The effect of thyroid hormone on atrial natriuretic factor (ANF) production was investigated in hypothyroid, euthyroid, and hyperthyroid rats by measuring levels of ANF mRNA and ANF in myocardium. ANF mRNA was quantitated by dot blot hybridization, and ANF by specific RIA. Relative ANF mRNA concentrations (ANF mRNA to 18S RNA) were determined for right atria, left atria, and ventricular apices. The total chamber content of ANF mRNA was estimated (concentration X total chamber RNA) and used as a measure of each tissue's synthetic capacity. For both atrial tissues, ANF mRNA contents were significantly higher in hyperthyroidism. In right atria, mean ANF mRNA contents in hypothyroidism and hyperthyroidism were 41% and 176%, respectively, of that in euthyroidism (P less than 0.05, by analysis of variance). Left atrial ANF mRNA contents in hypothyroidism and hyperthyroidism were 94% and 272%, respectively, of the euthyroid value (P less than 0.05). In contrast, atrial ANF mRNA concentrations did not differ significantly between thyroid states. In ventricle, ANF mRNA content and concentration were both correlated with serum T4 concentration. Ventricular ANF mRNA contents in hypothyroidism and hyperthyroidism were 31% and 178%, respectively, of that in euthyroidism (P less than 0.02). The concentration of ventricular ANF mRNA was also significantly increased in hyperthyroidism (P less than 0.05). Tissue content of ANF increased in the hyperthyroid right atria and decreased in the hyperthyroid left atria and ventricles. These observations suggest that increased ANF production by both atria and, to a lesser extent, by the ventricles contributes to the higher circulating ANF levels reported in hyperthyroidism. Furthermore, hyperthyroidism is associated with a specific increase in ventricular ANF mRNA expression as has been observed in other conditions causing ventricular hypertrophy.

Animals↗
PubMed1986

Hepatic glucose production and splanchnic glucose exchange in hyperthyroidism.

Hepatic glucose production (HGP) and net splanchnic glucose balance (NSGB) were simultaneously determined in the basal state in 8 hyperthyroid patients and 10 normal subjects using iv infusion of [3H]3-glucose and the hepatic venous catheter technique. Splanchnic glucose uptake (SGU) was calculated as the difference between the HGP and NSGB. SGU was also measured by determining the splanchnic extraction ratio of [3H]3-glucose across the splanchnic bed. In 5 hyperthyroid patients and 5 normal subjects a renal vein was also catheterized in the basal state. The influence of increased endogenous insulin secretion [stimulated by a low rate iv infusion of glucose (2 mg/kg . min)] on splanchnic and hepatic glucose exchange was also examined. Basal HGP (measured with [3H]3-glucose) was increased by 20% in the hyperthyroid patients [14.2 +/- 0.6 (SEM) mumol/kg . min] as compared to normal subjects (11.9 +/- 0.6, P less than 0.02). In marked contrast, NSGB output was slightly but not significantly decreased in the hyperthyroid group. SGU in the hyperthyroid patients, as determined with both techniques, was more than 2-fold higher than in the normal group (P less than 0.02-P less than 0.005). Splanchnic uptake of gluconeogenic precursors (lactate, pyruvate, glycerol) was increased by 20-120% in the patient group. During iv infusion of glucose, plasma insulin levels increased more in the hyperthyroid group (66% vs. 37%, P less than 0.05). Nevertheless, HGP and NSGB were less markedly suppressed in the patients as compared to the normal subjects (P less than 0.01), whereas the augmented SGU in the hyperthyroid patients reverted to normal. Splanchnic uptake of gluconeogenic precursors was unchanged in both groups. No net renal glucose production could be demonstrated in either group in the basal state. We conclude that in hyperthyroidism, increased HGP occurs in the face of an unchanged or slightly reduced rate of net glucose delivery to extrasplanchnic tissue. This discrepancy can be ascribed to augmented splanchnic uptake of glucose. These findings raise the possibility of futile cycling of glucose in the liver as a mechanism of increased oxygen consumption in hyperthyroidism. The data also demonstrate a diminished inhibitory effect of endogenous insulin on splanchnic glucose production, suggesting the presence of hepatic resistance to insulin in hyperthyroidism.

Adult↗
PubMed1991

Lipolytic and ketogenic fluxes in human hyperthyroidism.

The effect of hyperthyroidism on lipolytic and ketogenic fluxes was determined by measuring simultaneously (stable isotope methodology) glycerol, nonesterified fatty acids (NEFA), and ketone body (KB) kinetics in euthyroid and hyperthyroid subjects. In the postabsorptive state hyperthyroid patients had normal concentrations of insulin and glucagon, but increased concentrations (P less than 0.01) and turnover rates (P less than 0.01) of glycerol, NEFA, and KB. The ratio of NEFA appearance rate to glycerol appearance rate was decreased in hyperthyroid subjects (2.34 +/- 0.23 vs. 3.15 +/- 0.22; P less than 0.05), indicating that intracellular cycling between triglycerides and fatty acids was increased. The percentage of NEFA flux used for KB production, calculated from NEFA disappearance rates and KB appearance rates, was increased in hyperthyroid patients (21.20 +/- 2.75% vs. 13.37 +/- 0.63%; P less than 0.05), suggesting a diversion during hyperthyroidism of hepatic fatty acid metabolism toward ketogenesis. However, when the plasma NEFA levels of control subjects were raised by the infusion of a triglyceride emulsion to levels comparable to those observed in hyperthyroid patients their percentage of NEFA flux used for ketogenesis rose to values slightly higher (26.30%) than those of hyperthyroid subjects. In conclusion, 1) hyperthyroidism results not only in increased lipolysis, but also in enhanced triglyceride-fatty acid cycling, which could contribute to the excessive energy expenditure; and 2) the increased KB production of hyperthyroid patients results more from an increase in NEFA availability than from a direct stimulation of hepatic ketogenesis.

Adult↗