Experimental Hyperthyroidism Research Articles

Iron supplementation in experimental hyperthyroidism: effects on oxidative stress in skeletal muscle tissue.

This study was designed to investigate the effects of iron supplementation on the parameters of oxidative stress in the skeletal muscle tissue of hyperthyroidism induced rats. Hyperthyroidism was found to cause an increase in thiobarbituric acid-reactive substances (TBARS) and copper zinc superoxide dismutase (Cu, Zn SOD) activity, but decreases in the glutathione-peroxidase (GSH Px) activity and glutathione (GSH). Iron supplementation caused an increase in TBARS and a decrease in GSH. Iron supplementation in hyperthyroid rats attenuated the hyperthyroid state, but lowered the plasma ferritin level, which is considered an indicator of thyroid hormone action. Iron supplementation caused no additional increase in the TBARS in hyperthyroid rats, ameliorated the decrease in GSH content and abolished the induction of Cu, Zn SOD. Our findings suggested no increase, but a decrease, in the risk of oxidative stress in iron supplemented hyperthyroid rats. Whether supplementation of iron would have similar effects in humans should be further investigated in clinical studies.

Effects of Triiodothyronine and Estrogen Administration on Bone Mass, Mineral Content and Bone Strength in Male Rats

Experimental hyperthyroidism had a negative effect on bone mineral density, but did not significantly alter mechanical properties of femur and femoral bone thickness. Estradiol at a dose used in humans for the treatment of osteoporosis decreased seminal vesicle weight and concentration of testosterone but increased bone density in male rats compared to intact animals. In these rats, the mechanical analysis revealed an increased mechanical femur strength higher than the increase in bone density and femoral cortical thickness. When hyperthyroid male rats with low bone density were treated with estradiol in spite of a low plasma testosterone, the changes in bone density resulting from hyperthyroidism were entirely prevented. Estrogens protect the male skeleton against resorbing action of T (3). Treatment with estradiol in male rats with hyperthyroidism did not increase mechanical bone strength or femoral cortical thickness as it did with estradiol administration alone. Our results suggest that exogenously administered estrogens may have therapeutic value in preventing bone loss accompanying triiodothyronine administration, even in male rats with a low testosterone levels. At the concentration studied, estradiol increased in spite of low plasma testosterone, bone mineral density, mechanical strength of femur, and femoral cortical thickness.

Effects of Melatonin on Skeletal Muscle of Rats with Experimental Hyperthyroidism

The aim of this study was to investigate structural changes that occurred in the skeletal muscle of rats with experimental hyperthyroidism and the effect of melatonin on these changes. Groups of animals were designated as controls, 3,3′,5‐triiodothyronine (T3) injected and T3 + melatonin injected group. At the end of the study the tissue specimens were harvested and their structure examined. In the skeletal muscle of T3 injected rats a decrease was observed in muscle fiber diameter, splitting of fiber, collections of adipose tissue in perimysium, and gathering of nuclei in central compared to the control. Electron microscopic examination showed that mitochondria were dilated and the I band was less clear. In the T3 + melatonin injected group, the structure of fibers was similar to control. In conclusion, this study showed that T3 injection caused structural changes in the skeletal muscle and that melatonin had a positive effect on these changes.

Evoked Activity of Afferent and Efferent Fibers of the Sciatic Nerve in Rats under Conditions of Experimental Hyperthyroidism

In Wistar albino rats with experimental hyperthyroidism (HTh) and control animals, we measured parameters of the responses evoked in peripheral segments of the ventral and dorsal roots (VR and DR, respectively) by stimulation of the sciatic nerve. We found that the chronaxia of the afferent fibers of the sciatic nerve in HTh animals is shorter, while the duration of the mass action potential (AP) in the DR is somewhat longer than in the control. Under conditions of HTh, the excitation threshold of the efferent fibers became higher, the chronaxia decreased, and the second high-amplitude component could appear in the AP recorded from the VR. Possible mechanisms of changes in the excitability of afferent and efferent fibers of the sciatic nerve and specific features of the AP recorded from the VR under HTh conditions are discussed. In particular, we consider the possibility of ephaptic spreading of excitation in VR fibers under HTh conditions.

Thyroxine modulates corticotropin-releasing factor but not arginine vasopressin gene expression in the hypothalamic paraventricular nucleus of the developing Rat.

Neonatal rats were daily injected with 100 microg/kg T4 and killed at 4, 8 or 15 days. Circulating corticosterone and corticosteroid binding globulin concentrations increased in 8- and 15-day-old rats after T4 treatment. Plasma adrenocorticotropic hormone (ACTH) concentrations, pituitary ACTH content and pro-opiomelanocortin mRNA expression were unaffected in T4-treated rats. T4 treatment induced an increase in corticotropin-releasing factor (CRF) mRNA expression in the whole population of CRF synthesizing cells of the paraventricular nucleus (PVN) that became significant at day 8 and disappeared at day 15. Double labelling in situ hybridization revealed that CRF gene expression in the CRF+/arginine vasopressin (AVP)+ subpopulation was increased at days 4 and 8 and decreased at day 15. CRF immunoreactivity in the zona externa of the median eminence increased with age but was not affected by the experimental hyperthyroidism. The degree of CRF and AVP colocalization, the concentration of AVP mRNA in the parvo and magnocellular cell bodies of the PVN and the density of immunoreactive AVP in the zona interna or zona externa of the median eminence did not change after T4 treatment. Our data demonstrate that experimental hyperthyroidism accelerates the maturation of hypothalamic CRF gene expression, including in particular in the CRF+/AVP+ subpopulation, during the stress hyporesponsive period. These observations suggest that the physiological peak of plasma thyroxine that occurs between days 8-12 may participate in the maturation of hypothalamic CRF cells.

Renin-angiotensin system contribution to cardiac hypertrophy in experimental hyperthyroidism: an echocardiographic study.

The objective of this study was to evaluate, using echocardiography, the involvement of the renin-angiotensin system (RAS) in left ventricular (LV) hypertrophy development in experimental hyperthyroidism. Thyrotoxicosis was produced by a daily intraperitoneal injection of L-thyroxine (T4), 0.1 mg/kg per day for 15 days in Wistar rats. Control (euthyroid) rats received intraperitoneal daily injection of the thyroxine solvent. Two series of experiments were performed. In the first series, euthyroid (n = 10) and hyperthyroid (n = 14) rats were surgically prepared with a femoral artery catheter. After a 3-day recovery period, blood pressure and heart rate were measured and blood samples were collected in conscious and unrestrained rats. In the second series of experiment, measurement of LV geometry was realized with two-dimensional time-movement echocardiography on the 15th day of treatment in control conditions and after long-term treatment with the angiotensin II type I receptor antagonist valsartan (10 mg/kg per day for 15 days) in both euthyroid and hyperthyroid rats. The dose and duration of T4 treatment was sufficient to induce a significant degree of hyperthyroidism with characteristic features including tachycardia, systolic hypertension, myocardial hypertrophy, hyperthermia, and weight loss. In addition, we measured an increase in free fractions of thyroid hormones, and a threefold increase in plasma renin activity. Echocardiographic examinations in rats revealed a strong correlation between LV weight and echocardiographic LV mass. Hyperthyroid rats exhibited an increased LV mass with a marked increase in the LV end-diastolic posterior wall and septal thickness. Chronic treatment with valsartan prevented this concentric LV hypertrophy (p < 0.01), with full prevention of the LV posterior wall hypertrophy (p < 0.001) and decreased LV septal hypertrophy (p < 0.05). In conclusion, the cardiovascular alterations of hyperthyroidism were reproduced with thyroid hormone injections in rats. Activation of the RAS in hyperthyroid rats was accompanied by increased LV mass. Using valsartan, we demonstrated that the RAS impinged on the LV remodelling in our experimental hyperthyroidism model. A chronic treatment with an angiotensin II type I receptor antagonist prevented the development of the concentric LV hypertrophy associated with thyrotoxicosis.

Parameters of the Spinal Dorsal Surface Potential under Conditions of Experimental Hyperthyroidism

On Wistar rats with experimental hyperthyroidism (HTh) and a control group of the rats, we measured the parameters of the components of the spinal dorsal surface potentials (DSP) evoked by stimulation of the corresponding lumbar dorsal roots; the afferent spike (AS), N1-N3 components, and P wave were examined. After development of HTh, the amplitudes of all DSP components dramatically increased (by a factor from 1.8 to 3.1) with a simultaneous noticeable increase in the thresholds of the AS and N1-N3 DSP components and a drop in their chronaxia. Under the above conditions, there were no significant changes in the intensity of occlusion and characteristics of the heterosynaptic intersegmental interaction, while the intensity of presynaptic inhibition of the N1 DSP component decreased. Possible mechanisms of the observed modifications of the DSP parameters are discussed.

Selective modification of the pyruvate dehydrogenase kinase isoform profile in skeletal muscle in hyperthyroidism: implications for the regulatory impact of glucose on fatty acid oxidation.

The pyruvate dehydrogenase kinases (PDK1-4) regulate glucose oxidation through inhibitory phosphorylation of the pyruvate dehydrogenase complex (PDC). Immunoblot analysis with antibodies raised against recombinant PDK isoforms demonstrated changes in PDK isoform expression in response to experimental hyperthyroidism (100 microg/100 g body weight; 3 days) that was selective for fast-twitch vs slow-twitch skeletal muscle in that PDK2 expression was increased in the fast-twitch skeletal muscle (the anterior tibialis) (by 1. 6-fold; P<0.05) but not in the slow-twitch muscle (the soleus). PDK4 protein expression was increased by experimental hyperthyroidism in both muscle types, there being a greater response in the anterior tibialis (4.2-fold increase; P<0.05) than in the soleus (3.2-fold increase; P<0.05). The hyperthyroidism-associated up-regulation of PDK4 expression was observed in conjunction with suppression of skeletal-muscle PDC activity, but not suppression of glucose uptake/phosphorylation, as measured in vivo in conscious unrestrained rats (using the 2-[(3)H]deoxyglucose technique). We propose that increased PDK isoform expression contributes to the pathology of hyperthyroidism and to PDC inactivation by facilitating the operation of the glucose --> lactate --> glucose (Cori) and glucose --> alanine --> glucose cycles. We also propose that enhanced relative expression of the pyruvate-insensitive PDK isoform (PDK4) in skeletal muscle in hyperthyroidism uncouples glycolytic flux from pyruvate oxidation, sparing pyruvate for non-oxidative entry into the tricarboxylic acid (TCA) cycle, and thereby supporting entry of acetyl-CoA (derived from fatty acid oxidation) into the TCA cycle.

Experimental Hyperthyroidism Causes Inactivation of the Branched-Chain α-Ketoacid Dehydrogenase Complex in Rat Liver

Hyperthyroidism induced by 3-day treatment of rats with thyroid hormone (T3; 3,5,3′-triiodothyronine) at 0.1 or 1 mg/kg body wt/day resulted in a reduced activity state (% of enzyme in its active, dephosphorylated state) of the hepatic branched-chain α-ketoacid dehydrogenase (BCKDH) complex. One treatment with 0.1 mg T3/kg body wt caused a significant effect on the activity state of BCKDH complex after 24 h, indicating that the reduction of the activity state was triggered by the first administration of T3. Hyperthyroidism also caused a stable increase in BCKDH kinase activity, the enzyme responsible for phosphorylation and inactivation of the BCKDH complex, suggesting that T3 caused inactivation of the BCKDH complex by induction of its kinase. Western blot analysis also revealed increased amounts of BCKDH kinase protein in response to hyperthyroidism. No change in the plasma levels of branched-chain α-keto acids was observed in T3-treated rats, arguing against an involvement of these known regulators of BCKDH kinase activity. Inactivation of the hepatic BCKDH complex as a consequence of overexpression of its kinase may save the essential branched-chain amino acids for protein synthesis during hyperthyroidism.

Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism.

To study the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP). Thyrotoxicosis was produced by injections of L-thyroxine (0.5 mg/kg/day for five days). Blockers were atropine (0.5 mg/kg), atenolol (1 mg/kg) or prazosin (1 mg/kg). Eight animals were studied in each group. Spectral analyses was performed using continuous BP time series obtained in conscious rats. Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423+/-6 vs 353+/-4 bpm, P < 0.001, unpaired Student's t test), systolic BP elevation (142+/-3 vs 127+/-2 mmHg, P < 0.001) and cardiac hypertrophy (1.165+/-0.017 vs 1.006+/-0.012 g, P < 0.001). The intrinsic HR was markedly increased after treatment with thyroxine (497+/-16 vs 373+/-10 bpm, P < 0.05). Vagal tone was positively linearly related to intrinsic HR (r = 0.84, P< 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyroidism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (modulus 1.10+/-0.07 vs 1.41+/-0.06 mmHg, P < 0.01). Prazosin was without effect on this 0.4 Hz component in hyperthyroid animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in early experimental hyperthyroidism. The marked rise in the intrinsic HR could be the main determinant of tachycardia. The BP elevation may reflexly induce vagal activation and sympathetic (vascular and cardiac) inhibition.

Contribution of the autonomic nervous system to blood pressure and heart rate variability changes in early experimental hyperthyroidism

A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous system activity and thyroid hormones in the control of heart rate and blood pressure. We now report on thyrotoxicosis produced by daily intraperitoneal (i.p.) injection of l-thyroxine (0.5 mg/kg body wt. in 1 ml of 5 mM NaOH for 5 days). Control rats received i.p. daily injections of the thyroxine solvent. In order to estimate the degree of autonomic activation in hyperthyroidism, specific blockers were administered intravenously: atropine (0.5 mg/kg), prazosin (1 mg/kg), atenolol (1 mg/kg) or the combination of atenolol and atropine. A jet of air was administered in other animals to induce sympathoactivation. Eight animals were studied in each group. The dose and duration of l-thyroxine treatment was sufficient to induce a significant degree of hyperthyroidism with accompanying tachycardia, systolic blood pressure elevation, increased pulse pressure, cardiac hypertrophy, weight loss, tachypnea and hyperthermia. In addition, the intrinsic heart period observed after double blockade (atenolol+atropine) was markedly decreased after treatment with l-thyroxine (121.5±3.6 ms vs. 141.2±3.7 ms, P<0.01). Of the autonomic indices, vagal tone (difference between heart period obtained after atenolol and intrinsic heart period) was negatively linearly related to intrinsic heart period ( r=0.71, P<0.05). Atenolol modified neither the heart period nor blood pressure variability in rats with hyperthyroidism and in these rats the jet of air did not significantly affect the heart period level. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of blood pressure variability (analyses on 102.4 s segments, modulus 1.10±0.07 vs. 1.41±0.06 mm Hg, P<0.01) and prazosin was without effect on this 0.4 Hz component in these animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in early experimental hyperthyroidism. The marked rise in the intrinsic heart rate could be the main determinant of tachycardia. The blood pressure elevation may reflexly induce vagal activation and sympathetic (vascular and cardiac) inhibition.

Effect of chronic thyroxine treatment on pregnancy in rats: effects on oestrogen, progesterone, prolactin and gh receptors in uterus, liver and mammary gland

We have previously shown that experimental hyperthyroidism produces premature and difficult delivery and absence of lactation in spite of apparently adequate luteolysis and lactogenesis. To study the possible causes of these alterations we measured the effect of treatment with T4 (0.25 or 1 mg kg−1, s.c., daily, started 10-15 days before mating, HT0.25 and HT1) on serum hormones and their receptor (R) concentrations in reproductive tissues on day 20 of pregnancy (1800 hours), comparing them with controls on the same day (C20), or on day 21 of pregnancy (1800 hours) (C21). Serum prolactin (PRL) and corticosterone (B) concentrations increased in the HT groups, progesterone (Pg) and GH decreased and estradiol (E2) did not change, compared with C20 group. C21 rats had increased serum PRL and decreased Pg and GH. In HT rats mammary DNA and protein tissue content was doubled. Receptor concentrations were expressed per mg DNA. Mammary PRL-R were increased in HTI rats, while E-R and Pg-R were significantly lower in both HT groups. HT0.25 and HT1 rats had increased uterine E-R and Pg-R and decreased liver PRL-R and GH-R as well as their mRNAs. Liver E-R, PRL-R and GH-R were decreased in C21 rats, while uterine Pg-R were increased. Thus, some of the observed changes (serum Pg and GH, mammary and uterine Pg-R, and liver GH-R and PRL-R decreases and serum PRL increase) may be due at least partially to the advancement in luteolysis and delivery, being similar to the changes observed between days 20 and 21. The changes in serum B, mammary PRL-R, and mammary and uterine E-R may be caused solely by the T4 treatments and may play a role in the alterations previously observed.

Some physiological reactions stimulated by isadrine in experimental hyperthyroidism in rats

The chronotropic, calorigenic, and thermogenic effects of isopropyl noradrenalin (INA) and of the vapor mixture of INA and propranolol were studied in 86 adult male albino rats over the course of development of hyperthyrosis induced by 1 to 12 injections of triiodothyronin in a dose of 100 \xg/kg. The Pl-adrenergic reaction of the heart and the calorigenic and thermogenic reactions undergo several phases upon stimulation with isadrin in a dose of 2.0 pg/kg/min: latent period, period of high reactivity, and period of reduction of this activity. The efficacy of inderal (25 \ig/kg/min) adrenoblocking of the positive chronotropic effect of exogenously administered isadrin decreases with the progress of hyperthyrosis.

The effect of iron supplementation on GSH levels, GSH-Px, and SOD activities of erythrocytes in L-thyroxine administration.

Our aim was to study the effect of iron supplementation on the following aspects of erythrocyte metabolism in experimental hyperthyroidism: glutathione (GSH) levels, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities. Hyperthyroidism induced by L-thyroxine administrations significantly raised erythrocyte GSH, GSH-Px and SOD levels of the rats (P < 0.001). Likewise, we observed that iron supplementation induced significant rises in erythrocyte GSH, GSH-Px and SOD levels (P < 0.001) as compared with the control group. The erythrocyte GSH, GSH-Px and SOD levels of hyperthyroidism-induced iron-supplemented animals were significantly higher when compared with either the iron-supplemented group (P < 0.001) or the only L-thyroxine-administered hyperthyroid group (P < 0.001, P < 0.05, P < 0.01, respectively). The results of this study show that L-thyroxine administration and/or iron supplementation increases GSH, GSH-Px and SOD levels of erythrocytes.

Calcium, magnesium, and zinc status in experimental hyperthyroidism.

In this study, experimental hyperthyroidism was established and used to investigate possible alterations in the calcium (Ca), magnesium (Mg), and zinc (Zn) homeostasis by assessing their concentrations in plasma and erythrocytes. In the L-thyroxine-induced hyperthyroidism condition, the experimental animals show a significant decrease in erythrocyte Ca, Mg, and Zn concentrations, and a significant decrease in plasma Mg concentration. Significant positive correlations were found for Mg and Zn both in plasma and in erythrocytes. The results suggest that the homeostasis of Ca, Mg, and Zn is altered during experimental hyperthyroidism.

The influence of experimental hyperthyroidism on responsiveness in rabbit aortic smooth muscle

This study investigated the responsiveness of hyperthyroid and control (euthyroid) rabbit aortic rings to vasoconstrictor agents. There was no significant difference between the responsiveness of hyperthyroid and control tissues to KCl. Maximum responses ( E m) to noradrenaline and serotonin were reduced in hyperthyroid rabbit aortic rings compared to those euthyroid rings. The sensitivity (i.e., EC 50) of hyperthyroid aortic rings to noradrenaline and serotonin compared to euthyroid controls was unchanged. The K b value of prazosin against 10 −6 M noradrenaline-induced contractions in eu- and hyperthyroid states was 1.97 ± 0.59 · 10 −9 M and 1.92 ± 0.79 · 10 −9 M, respectively. The K b value of methisergide against 10 −6 M serotonin-induced contractions in eu- and hyperthyroid states was 1.46 ± 0.80 · 10 −9 M and 1.10 ± 0.16 · 10 −9 M, respectively. These data indicate that vascular reactivity is altered in experimental hyperthyroidism and this alteration, if any, do not occur at the receptor level.

The Effects of Experimental Hyperthyroidism and Hypothyroidism on the Isometric Contraction Properties of Plantaris Muscle in Rats, the Relationship Between These Properties and Capillarity

In this study, the isometric properties and the capillarity of isolated plantaris muscle in hyperthyroid and hypothyroid rats and the relation between these parameters have been investigated. The experiment was carried out in 3 groups as control, hyperthyroidism and hypothyroidism. Each group comprised of 20 Wistar albino adult female rats. In anaesthetized rats, single and tetanic stimulations were applied directly to the plantaris muscle in an isolated tissue bath. From the recordings obtained by an isometric transducer and a polygraph, contraction time, half relaxation time, twitch tension and tetanic force were measured. The plantaris muscle of the other leg was prepared in paraffin blocks after fixation in neutral formalin. 5 \mum sections taken from the blocks were stained by haematoxylin and eosin and their capillary densities were determined under light microscope. No significant difference was found in the contraction time between the hyperthyroid and the hypothyroid groups. Half relaxation time decreased in the hyperthyroid group while it increased in the hypothyroid group. Twitch tension and tetanic force decreased in the hyperthyroid group and increased in the hypothyroid group. No difference was found in the capillary density of plantaris muscle between the groups. There was also a lack of correlation between the capillary density of the muscle and the twitch tension and the tetanic force of the muscle in both the hyperthyroid and the hypothyroid groups.

Antioxidant status in experimental hyperthyrodism: effect of vitamin E supplementation

Free radical-mediated oxidative stress has been implicated in the genesis and exacerbation of degenerative diseases. In view of the role of oxidative processes in hyperthyroidism, in this study, we investigated the antioxidant status of erythrocytes in experimental hyperthyroidism and the effect of vitamin E supplementation on defense systems. Our findings of significantly increased T 4 and T 3 and undetectable TSH values in thyroxine administered rats confirmed the establishment of hyperthyroidism. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) values were found to be significantly increased in hyperthyroid rats in comparison to the control group. Vitamin E supplementation to hyperthyroid rats induced a significant decrease in GSH-Px activity and a significant increase in GSH level. These findings show that hyperthyroidism increases the components of the antioxidant system in the erythrocytes. Furthermore, vitamin E supplementation reduces the burden of oxidative stress in hyperthyroidism.

Early changes in plasma glucagon and growth hormone response to oral glucose in experimental hyperthyroidism

The mechanisms underlying deterioration of glucose tolerance associated with hyperthyroidism are not completely understood. Increases in glucagon and growth hormone (GH) secretion have been previously found in hyperthyroid subjects, and could play a crucial role in this phenomenon. However, studies have not yet established the time sequence of changes in plasma glucose on the one hand and glucagon and GH on the other. To assess the early effects of thyroid hormone excess on glucose tolerance and plasma concentrations of the main glucoregulatory hormones, 12 nondiabetic euthyroid subjects underwent an oral glucose tolerance test (OGTT) before and after triiodothyronine ([T 3] 120 μg/d) was administered for 10 days. Plasma levels of glucose, insulin, glucagon, and GH were determined at fasting and after the glucose load. T 3 administration caused a marked increase in serum T 3 (8.8 ± 0.6 v 2.0 ± 0.1 nmol/L), with clinical and biochemical signs of thyrotoxicosis. During the treatment, plasma glucose significantly increased both at fasting and after the glucose load (basal, 5.3 ± 0.1 v 4.9 ± 0.2 mmol/L, P < .05; area under the curve [AUC] for OGTT, 7.7 ± 0.3 v 6.7 ± 0.4 mmol/L · min, P < .01) without any change in plasma insulin levels. After T 3 administration, plasma glucagon levels were lower than at baseline (basal, 92 ± 7 v 148 ± 35 ng/L; AUC, 74 ± 6 v 98 ± 16 ng/L · min, P < .05), showing an appropriate reduction by the increased glucose levels. Conversely, plasma GH showed impaired suppression by hyperglycemia (AUC, 1.2 ± 0.3 v 0.7 ± 0.2 μg/L · min, P < .05). In conclusion, thyroid hormone excess rapidly impairs glucose tolerance. Altered secretion of GH is an early event in thyrotoxicosis accompanying the onset of hyperglycemia, whereas plasma glucagon is appropriately suppressed by the increased plasma glucose levels. Thus, GH but not glucagon may contribute to the early hyperglycemic effect of thyrotoxicosis.

Lipid peroxidation and vitamin E supplementation in experimental hyperthyroidism

Lipid peroxidation and vitamin E supplementation in experimental hyperthyroidism