glycogen and Hyperthyroidism

Topics: Adipocytes; Animals; Glucose; Glucose-6-Phosphatase; Glycogen; Humans; Hyperthyroidism; Insulin; Insulin Resistance; Insulin Secretion; Lipid Metabolism; Liver; Monosaccharide Transport Proteins; Muscle, Skeletal; Nuclear Proteins; Oligonucleotide Array Sequence Analysis; Protein Serine-Threonine Kinases; Proteins; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Receptors, Adrenergic, beta-2; Thyroid Hormones; Transcription Factors

Topics: Acetylcholine; Adenine Nucleotides; Caffeine; Calcium; Catecholamines; Glycogen; Guanethidine; Heart; Hyperthyroidism; Isoproterenol; Monoamine Oxidase Inhibitors; Myocardium; Norepinephrine; Perfusion; Pharmacology; Phosphorylase Kinase; Piperazines; Research; Reserpine; Strophanthins; Sympathetic Nervous System; Theophylline; Tyramine

Hyperthyroidism is known to increase food intake and central administration of thyroid hormone shows acute orexigenic effects in rodents. We investigated whether T3 influences appetite and glucose homeostasis by modulating circulating ghrelin, an important orexigenic hormone, in Zucker fatty rats. The acute anorectic effects of T3 and ghrelin mimetic MK-0677 were studied in rats trained for fasting induced food intake. The serum concentration of T3, ghrelin, glucose, triglycerides, and liver glycogen were estimated. The involvement of sympathetic nervous system was evaluated by conducting similar experiments in vagotomized rats. T3 increased food intake and glucose in rats over 4 h, with increase in serum T3 and decrease in liver glycogen. T3 treatment was associated with increase in serum ghrelin. An additive effect on appetite and glucose was observed when T3 (oral) was administered with central (intracerebroventricular) administration of a ghrelin mimetic, MK-0677. Ghrelin antagonist, compound 8a, antagonized the hyperglycemic and hyperphagic effects of T3. In vagotomized rats, T3 did not show increase in appetite as well as glucose. Serum ghrelin levels were unchanged in these animals after T3 treatment. However, T3 showed increase in serum triglyceride levels indicating its peripheral lipolytic effect, in vagotomized as well as sham treated animals. To conclude, acute orexigenic and hyperglycemic effects of T3 are associated with ghrelin secretion and activity. This effect seems to be mediated via vagus nerves, and is independent of glucoregulatory hormones.

Topics: Animals; Appetite Regulation; Blood Glucose; Disease Models, Animal; Eating; Feeding Behavior; Ghrelin; Glycogen; Homeostasis; Hyperphagia; Hyperthyroidism; Indoles; Injections, Intraperitoneal; Injections, Intraventricular; Liver; Male; Rats, Zucker; Spiro Compounds; Time Factors; Triglycerides; Triiodothyronine; Vagotomy; Vagus Nerve

Thyroid dysfunction can compromise physical capacity. Here, we analyze the effects of hyperthyroidism and hypothyroidism on maximum swim time in rats subjected to acute forced swimming, as an indicator of anaerobic capacity. Animals were forced to swim against a load (5% of body weight) attached to the tail and were killed 48 hours after the last test. Hyperthyroid rats were treated with thyroxine (50 mug/100 g body weight, i. p. for 7 days). The hypothyroid group received 0.03% methimazole in the drinking water for 4 weeks. Thyroid state was confirmed by alterations in serum thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), and liver mitochondrial glycerol phosphate dehydrogenase (mGPD) activity. Hyperthyroid rats presented significantly lower visceral fat mass (VFM) and higher food intake (p<0.05) with unchanged body weight. Maximum swim time (MST), glycogen content (skeletal muscle and liver), and leptin levels were lower while corticosterone was higher (p<0.05). In hypothyroid rats body weight was lower (p<0.05), without changes in VFM. Tested at 7-day intervals, MST was lower for tests 2, 3, and 4 (p<0.05). Muscle glycogen was higher in extensor digitorum longus (EDL) and soleus (p<0.05), without changes in liver. Serum corticosterone was lower, while leptin was higher (p<0.05). These results suggest that in hyperthyroid and hypothyroid rats, thyroid hormones together with corticosterone and/or leptin may impair exercise capacity differently through its known effects on glycogen metabolism.

Topics: Animals; Body Composition; Corticosterone; Eating; Exercise Tolerance; Glycogen; Hyperthyroidism; Hypothyroidism; Leptin; Liver Glycogen; Male; Muscle, Skeletal; Rats; Rats, Wistar; Swimming; Thyrotropin; Thyroxine

1. The efficacy of coumarin (1,2-benzopyrone) was examined for the regulation of hyperthyroidism in female rats. 2. Coumarin was administered (10 mg/kg per day for 15 days) to l-thyroxine (L-T(4))-induced hyperthyroid as well as to euthyroid rats and changes in serum concentrations of thyroid hormones and in associated parameters, such as serum cholesterol, activity of hepatic 5'-monodeiodinase (5'DI) and glucose-6-phosphatase (G-6-Pase), glycogen content, bodyweight and daily food consumption, were analysed. Simultaneously, changes in hepatic lipid peroxidation (LPO), reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were also investigated. 3. Although L-T(4) administration increased serum levels of thyroid hormones, the activity of hepatic 5'DI, G-6-Pase and LPO and daily food consumption, it decreased the level of serum cholesterol, hepatic glycogen content and the activities of anti-oxidant enzymes, such as SOD, CAT and GSH. 4. However, simultaneous administration of coumarin for 15 days to a group of hyperthyroid animals reversed most of the aforementioned changes, indicating its potential to ameliorate hyperthyroidism. Moreover, the drug did not increase, but rather decreased, hepatic LPO, suggesting its safe nature. 5. The present findings reveal a positive role for coumarin in the regulation of hyperthyroidism without any hepatotoxicity. It also appears that the test compound inhibits thyroid function at both a glandular level and at the level of peripheral conversion of T(4) to tri-iodothyronine.

Topics: Animals; Antithyroid Agents; Body Weight; Catalase; Cholesterol; Coumarins; Disease Models, Animal; Eating; Female; Glucose-6-Phosphatase; Glutathione; Glycogen; Hyperthyroidism; Iodide Peroxidase; Lipid Peroxidation; Liver; Rats; Rats, Wistar; Superoxide Dismutase; Thyroid Gland; Thyroid Hormones; Thyroxine; Time Factors

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.

Topics: Adipose Tissue; Animals; Blood Vessels; Body Weight; Glycogen; Hyperthyroidism; Male; Mast Cells; Melatonin; Mitochondria; Muscle Fibers, Skeletal; Muscle, Skeletal; Rats; Rats, Wistar; Triiodothyronine

This study was undertaken to define the contributions of left ventricular hypertrophy (LVH) and increased adrenergic activity to the acceleration of ischemic contracture (IC) that occurs in chronic hyperthyroid rat heart. Acute and chronic hyperthyroidism (THYR) were induced by thyroxine administration for 2 and 14 days, respectively, and normal animals (NORM) served as controls. Isolated hearts were perfused in a Langendorff mode. NORM alpha acute, n = 6; THYR alpha acute, n = 8; and THYR alpha, n = 13; and NORM alpha, n = 13 were subjected to 20-min zero-flow global ischemia (I) and 45-min reperfusion (R). Additional THYR and NORM hearts treated with propranolol (prop) were subjected to 30-min I; THYR beta prop, n = 6 and NORM beta prop, n = 8, and THYR beta, n = 6, NORM beta, n = 8 served as controls. Acceleration of IC was measured by the time to peak contracture (Tmax). Left ventricular hypertrophy (LVH) was assessed by the ratio of left ventricular weight in milligrams (LVW) to animal body weight (BW) in grams. Cardiac hypertrophy developed in chronic but not acute hyperthyroidism. Propranolol reduced the extent of LVH. Contracture occurred earlier in chronic than in acute hyperthyroid and normal hearts. Propranolol did not alter contracture. In conclusion, IC is accelerated by thyroxine administration, and this is probably not due to LVH or increased beta-adrenergic activity. Propranolol diminishes LVH in hyperthyroidism.

Topics: Adrenergic beta-Antagonists; Animals; Glycogen; Hyperthyroidism; Hypertrophy, Left Ventricular; Male; Myocardial Contraction; Myocardial Ischemia; Myocardial Reperfusion; Propranolol; Rats; Rats, Wistar

Yangyin Anshen Koufuye could obviously decrease the spontaneous activity of rats, effectively shorten the process of falling into sleep of normal rats which were injected pentobarbital sodium and prolong the sleeping time. The effect of sedation and hypnotism were the same as Zhaoren Anshen Koufuye. Yangyin Anshen Koufuye also could markedly reduce the serum tensity of T3, T4 of hyperthyroid rats, which equaled to TCM's deficiency of yin. It also could prevent the glycogen content of liver from decreasing, decrease heart rate, resist weight losing, thus to show the effect of nourishing Yin and tranquilizing.

Topics: Animals; Behavior, Animal; Drug Combinations; Drugs, Chinese Herbal; Female; Glycogen; Hyperthyroidism; Liver; Male; Mice; Phytotherapy; Plants, Medicinal; Rats; Rats, Sprague-Dawley; Rehmannia; Thyroxine; Triiodothyronine; Yin Deficiency; Ziziphus

Changes in thyroid status affect metabolism not only directly, but influence it also by alterations in insulin secretion and action. Despite several investigations, these effects are, however, poorly characterised or even controversial. The aim of the studies was to investigate the effect of hyperthyreosis (HT) and hypothyreosis (HPT) on insulin binding by rat liver membranes. Some metabolic parameters reflecting insulin and thyroid hormones action were also determined. HT and HPT were developed by daily administration for 3 weeks of thyroxine (T (4) ) and thiouracil (TU), respectively. Experimental hyperthyreosis and hypothyreosis caused deep changes in metabolism. The greatest alterations were observed in body and thyroid glands weight, blood triiodothyronine (T (3) ), T (4), glucose, and insulin levels, liver glycogen amount and number of insulin receptors. HT reflected in rats in slower rate of growth and in smaller thyroid glands weight. In comparison to controls, T (4) concentration in HT was almost doubled and it was reduced by about 30% in HPT. Also, T(3), insulin and glucose levels in HT were heightened. Simultaneously, binding of insulin to liver membranes was elevated in HT and reduced in HPT. In HT the number of high affinity insulin receptors (HAIRs) and low affinity insulin receptors (LAIRs) was increased, whereas in HPT the amount of HAIRs was diminished. HT caused a drastic reduction of glycogen concentration in liver, but no changes were observed for muscle glycogen. Considering lipid metabolism, only free fatty acids (FFA) level in blood was changed (in HPT), but no differences were observed in serum concentration of triglycerides and cholesterol. Several metabolic changes observed in HT and HPT seem to be the dire ct consequence of alterations of thyroid hormone concentrations. These disturbances, together with the direct effect of HT or HPT on insulin secretion, binding and action lead, in turn, to changes in the other metabolic parameters. As a result of these disturbances the adaptive mechanisms appear. One of them is change in the number of insulin membrane receptors taking place even against the well known "down-regulation" theory.

Topics: Animals; Antithyroid Agents; Cholesterol; Fatty Acids, Nonesterified; Glucose; Glycogen; Hyperthyroidism; Hypothyroidism; Insulin; Liver; Male; Protein Binding; Rats; Rats, Wistar; Receptor, Insulin; Thiouracil; Thyroxine; Triglycerides

The effects of insulin on the rates of glucose disposal were studied in soleus muscles isolated from hyper- or hypothyroid rats. Treatment with triiodothyronine for 5 or 10 days decreased the sensitivity of glycogen synthesis but increased the sensitivity of lactate formation to insulin. The sensitivity of 3-O methylglucose to insulin was increased only after 10 days of treatment and was accompanied by an increase in the sensitivity of 2-deoxyglucose phosphorylation; however, 2-deoxyglucose and glucose 6-phosphate in response to insulin remained unaltered. In hypothyroidism, insulin-stimulated rates of 3-O-methylglucose transport and 2-deoxyglucose phosphorylation were decreased; however, at basal levels of insulin, 3-O-methylglucose transport was increased, while 2-deoxyglucose phosphorylation was normal. In these muscles, the sensitivity of lactate formation to insulin was decreased; this defect was improved after incubation of the muscles with prostaglandin E2. The results suggest: (a) in hyperthyroidism, insulin-stimulated rates of glucose utilization in muscle to form lactate are increased mainly because of a decrease in glycogen synthesis; when hyperthyroidism progresses in severity, increases in the sensitivity of glucose transport to insulin and in the activity of hexokinase may also be involved; (b) in hypothyroidism, the decrease in insulin-stimulated rates of glucose utilization is caused by decreased rates of glycolysis; (c) prostaglandins may be involved in the changes in sensitivity of glucose utilization to insulin observed in muscle in altered thyroid states.

Topics: Animals; Biological Transport, Active; Cortisone; Dinoprostone; Drug Interactions; Glucose; Glycogen; Glycolysis; Growth Hormone; Hyperthyroidism; Hypothyroidism; In Vitro Techniques; Insulin; Lactic Acid; Male; Muscle, Skeletal; Phosphorylation; Rats; Rats, Wistar; Triiodothyronine

The effects of alterations in thyroid status on glucose metabolism have been investigated in rat hepatocytes. Addition of 10 or 40 mmol/L glucose induced increases in respiration rate that were significantly larger in cells from hyperthyroid rats than from hypothyroid animals. The responses of hepatocytes from euthyroid rats were intermediate. In cells from hyperthyroid rats, most of the increase occurred upon addition of 10 mmol/L glucose, with only a further small stimulation resulting when glucose concentration was increased to 40 mmol/L. For a given glucose concentration, glycolytic rates, determined by measuring release of tritium from [6-3H]glucose, were comparable in all thyroid states. Studies with 10 mmol/L [2-3H]glucose showed that cycling between glucose-6-phosphate and glucose was almost twofold higher in euthyroid and hyperthyroid states as compared with the hypothyroid state, although the magnitude of the increase in cycling rate was only approximately 0.2 mumol glucose.min-1.g-1. When 40 mmol/L [2-3H]glucose was added, over 44% of the glucose that was phosphorylated to glucose-6-phosphate was cycled back to glucose, but this cycling was independent of thyroid status. Cycling between fructose-1,6-bisphosphate and fructose-6-phosphate was negligible in all thyroid states. Rates of glycogen synthesis were comparable in hypothyroid and hyperthyroid states and slightly less than in the euthyroid state. Glycolytically formed pyruvate was cycled back to glucose in hepatocytes from hypothyroid, euthyroid, and hyperthyroid rats. During a 60-minute incubation period, cycling to glucose in the presence of 10 mmol/L or 40 mmol/L glucose was up to twofold higher in cells from euthyroid and hyperthyroid rats than in hepatocytes from hypothyroid animals. The measured increases in cycling rates induced by thyroid hormone were small and in theory could have been satisfied by a much smaller increase in respiration rate than was observed.

Topics: Animals; Dose-Response Relationship, Drug; Fructosediphosphates; Fructosephosphates; Glucose; Glucose-6-Phosphate; Glucosephosphates; Glycogen; Hyperthyroidism; Hypothyroidism; Lactates; Liver; Oxidation-Reduction; Oxygen Consumption; Phosphorylation; Pyruvates; Pyruvic Acid; Rats; Thyroid Gland; Tritium

Experimental hyperthyroidism induced by the administration of tri-iodothyronine (T3; 100 micrograms/100 g body wt; 3 days) increased plasma non-esterified fatty acids in the fed state in the rat. At the same time, hepatic PDH kinase responded with a persistent (1.6-fold) increase in activity. The exposure of hepatocytes from fed euthyroid rats to T3 (100 nM) in culture for 21 h increased PDH kinase activity to an extent comparable to that observed in vivo in response to hyperthyroidism. The in vitro increase in PDH kinase activity was suppressed by insulin (100 microU/ml) and by inhibition of mitochondrial fatty acid oxidation. The results demonstrate a direct hepatic action of T3 to increase PDH kinase activity, which is mediated by intramitochondrial fatty acyl-CoA or a product of beta-oxidation, and facilitated by hepatic insulin resistance.

Topics: Acyl Coenzyme A; Animals; Blood Glucose; Bucladesine; Carnitine O-Palmitoyltransferase; Cells, Cultured; Cyclic AMP; Eating; Enzyme Inhibitors; Fatty Acids, Nonesterified; Female; Glucagon; Glycogen; Hyperthyroidism; Insulin; Liver; Mitochondria; Oxidation-Reduction; Palmitates; Protein Kinases; Protein Serine-Threonine Kinases; Pyruvate Dehydrogenase Acetyl-Transferring Kinase; Rats; Rats, Wistar; Triglycerides; Triiodothyronine

The effect of calcium activation on energy production was investigated in isolated perfused hearts from rats treated with triiodothyronine (T3) during 15 days (0.2 mg/kg/day) and in hearts of rats allowed to recover after T3-treatment during 15 days. Changes in phosphorylated compound concentrations were followed in the isolated hearts perfused with a glucose-pyruvate medium by 31P-NMR spectroscopy, when the external calcium concentration was increased from 0.5-1, 1.5 and 2 mM. As expected, T3-treatment resulted in the hypertrophy of the heart (50% increase in HW/BW) that was nearly reversible 15 days after discontinuation of the treatment. When compared to controls, creatine, phosphocreatine (PCr) and glycogen contents were lower (58, 24 and 17% decrease respectively) in the hypertrophied hearts and higher (10, 14 and 18% respectively) after regression of hypertrophy. Intracellular pH, ATP, inorganic phosphate concentrations and the phosphorylation potential were not altered under T3-treatment and after regression of hypertrophy, while calculated free ADP concentration was lower in hypertrophied hearts (control: 40 +/- 2 microM, T3-treatment: 21 +/- 1 microM, regression: 37 +/- 1 microM). Increasing the calcium concentration induced a similar increase in left ventricular developed pressure in the three groups of hearts, with inorganic phosphate concentration increasing with cardiac work. The PCr concentration slightly decreased while the ATP concentration did not change. In spite of different initial PCr concentrations, the evolutions of PCr and Pi concentrations for each stepwise increase in external calcium were similar in the three groups. It is concluded that, in spite of the well-known decrease in efficiency induced by the drug, the mechanisms of PCr (ATP) production remain able to respond to an acute moderate increase in energy demand provoked by a physiological stimulus. This adaptation also persists after the treatment when the energy metabolism balance is apparently improved.

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Animals; Calcium; Cardiomegaly; Creatine; Energy Metabolism; Female; Glycogen; Heart; Hyperthyroidism; Magnetic Resonance Spectroscopy; Myocardial Contraction; Myocardium; Organ Size; Phosphates; Phosphocreatine; Rats; Rats, Sprague-Dawley; Triiodothyronine; Ventricular Pressure

The influence of hyperthyroidism on the action of drugs affecting rat liver glycogen content and its mechanism were investigated. The thyroid-induced hyperthyroidism of rat served as the model. In normal rats, dexamethasone (5 mg.kg-1, ip) increased the content of liver glycogen and decreased the Bmax of glucocorticoid receptors (GCR) in liver cytosol. These effects were minimized or even disappeared in hyperthyroid rat models. On the other hand, in normal rats, epinephrine (0.20 mg.kg-1, ip) decreased the content of liver glycogen. This effect was potentiated in hyperthyroid rat models. Epinephrine did not affect the Bmax of GCR in liver cytosol of normal and hyperthyroid rats. These results suggested that hyperthyroidism may be one of the causes effecting the individual differences of drug action, and that the influence of hyperthyroidism on the glycogen-increasing action of dexamethasone correlated well with the changes in glucocorticoid receptor. The mechanism of the influence of hyperthyroidism on the glycogen-decreasing action of epinephrine is to be further explored.

Topics: Animals; Cytosol; Dexamethasone; Epinephrine; Glycogen; Hyperthyroidism; Liver; Male; Oxygen Consumption; Rats; Rats, Wistar; Receptors, Glucocorticoid

1. The actions of the beta-adrenoceptor agonist isoprenaline on glucose and glycogen metabolism, in the presence of various concentrations of insulin, were investigated in isolated soleus muscle preparations taken from eu-, hyper- and hypothyroid rats. 2. Hyperthyroidism, induced by 3,3',5-tri-iodo-D-thyronine (T3) administration for 5 days, increased the rate of lactate formation and suppressed the rate of glycogen synthesis in soleus muscle in response to isoprenaline, even in the presence of physiological or supraphysiological insulin concentrations. 3. Hypothyroidism, induced by administration of 6-n-propyl-2-thiouracil for 4 weeks, decreased the rate of isoprenaline-stimulated lactate formation at all insulin concentrations, but significantly decreased the responsiveness of lactate formation only at low insulin concentrations. In the presence of 100 or 10,000 mu-units of insulin/ml, the ability of isoprenaline to suppress the rate of glycogen synthesis was markedly impaired (inhibition at 100 mu-units of insulin/ml and 1 micro-M-isoprenaline: eu- 72.6 +/- 2.9%; hypo-41.0 +/- 2.1%; P less than 0.001). 4. Hyperthyroidism had no effect on the number or affinity of beta-adrenoceptors, defined by 125I-pindolol binding, or beta-adrenoceptor- or forskolin-stimulated adenylate cyclase activity in membrane preparations of gastrocnemius muscle, whereas hypothyroidism increased the beta-adrenoceptor density and decreased the beta-adrenoceptor-stimulated adenylate cyclase activity, without affecting the receptor affinity or forskolin-stimulated adenylate cyclase activity. 5. It is concluded that there is a complex interplay between insulin, catecholamines and thyroid hormones to regulate skeletal-muscle glucose metabolism. The changes observed in muscles in hypothyroidism may be explained, at least in part, by changes in beta-adrenoceptor-G-protein-adenylate cyclase coupling affecting the generation of cyclic AMP and the regulation of some of the key enzymes of glycogen metabolism; in contrast, the changes observed in muscles in hyperthyroidism do not appear to result from alterations at the level of the receptor-mediated second-messenger generation.

Topics: Adrenergic beta-Agonists; Animals; Glucose; Glycogen; Hyperthyroidism; In Vitro Techniques; Insulin; Isoproterenol; Lactates; Male; Muscles; Radioligand Assay; Rats; Rats, Inbred Strains; Thyroid Gland

Topics: Animals; Eating; Glucose; Glycogen; Hyperthyroidism; Kinetics; Muscles; Rats; Rats, Inbred Strains; Starvation

In the fed state, hyperthyroidism increased glucose utilization indices (GUIs) of skeletal muscles containing a lower proportion of oxidative fibres. Glycogen concentrations were unchanged, but active pyruvate dehydrogenase (PDHa) activities were decreased. Hyperthyroidism attenuated the effects of 48 h of starvation to decrease muscle GUI. Glycogen concentrations and PDHa activities after 48 h of starvation were low and similar in euthyroid and hyperthyroid rats. The increase in glucose uptake and phosphorylation relative to oxidation and storage in skeletal muscle induced by hyperthyroidism may contribute to increased glucose re-cycling in the fed hyperthyroid state and to glucose turnover in the starved hyperthyroid state.

Topics: Animals; Blood Glucose; Fatty Acids, Nonesterified; Female; Food; Glucose; Glycogen; Hyperthyroidism; Insulin; Muscles; Oxidation-Reduction; Phosphorylation; Pyruvate Dehydrogenase Complex; Pyruvates; Pyruvic Acid; Rats; Rats, Inbred Strains; Starvation; Triiodothyronine

The influence of the maternal thyroid status on the fetal and neonatal myocardial protein, carbohydrate and lipid metabolism was studied in rats. The neonates born of hypothyroid mothers could not survive beyond 8 days after birth. The offsprings born of hypothyroid mothers showed growth retardation, decreased level of heart mitochondrial protein, reduced myocardial free fatty acid (FFA) oxidation at birth and afterwards, low glucose oxidation by the heart at later fetal stages, and afterwards, despite low heart glycogen reserve, glucose oxidation was high. The offsprings born of hyperthyroid mothers showed stimulation in overall growth, increased myocardial FFA oxidation and increased 14C-glucose incorporation into glycogen as well as increased myocardial glucose oxidation during fetal stages. Results indicate that maternal thyroid hormones play an important role in the metabolic control of fetuses and neonates.

Topics: Animals; Animals, Newborn; Body Weight; Female; Fetal Heart; Glucose; Glycogen; Hyperthyroidism; Hypothyroidism; Lipid Metabolism; Maternal-Fetal Exchange; Pregnancy; Pregnancy Complications; Proteins; Rats; Rats, Inbred Strains; Thyroid Gland; Thyroxine

1. The effects of hypothyroidism (caused by surgical thyroidectomy followed by treatment for 1 month with propylthiouracil) and of hyperthyroidism [induced by subcutaneous administration of L-tri-iodothyronine (T3)] on glucose tolerance and skeletal-muscle sensitivity to insulin were examined in rats. Glucose tolerance was estimated during 2 h after subcutaneous glucose injection (1 g/kg body wt.). The sensitivity of the soleus muscle to insulin was studied in vitro in sedentary and acutely exercised animals. 2. Glucose tolerance was impaired in both hypothyroid and hyperthyroid rats in comparison with euthyroid controls. 3. In the soleus muscle, responsiveness of the rate of lactate formation to insulin was abolished in hypothyroid rats, whereas the sensitivity of the rate of glycogen synthesis to insulin was unchanged. In hyperthyroid animals, opposite changes were found, i.e. responsiveness of the rate of glycogen synthesis was inhibited and the sensitivity of the rate of lactate production did not differ from that in control sedentary rats. 4. A single bout of exercise for 30 min potentiated the stimulatory effect of insulin on lactate formation in hyperthyroid rats and on glycogen synthesis in hypothyroid animals. 5. The data suggest that thyroid hormones exert an interactive effect with insulin in skeletal muscle. This is likely to be at the post-receptor level, inhibiting the effect of insulin on glycogen synthesis and stimulating oxidative glucose utilization.

Topics: Animals; Glucose Tolerance Test; Glycogen; Hyperthyroidism; Hypothyroidism; In Vitro Techniques; Insulin; Lactates; Male; Muscles; Physical Conditioning, Animal; Rats; Rats, Inbred Strains; Thyroid Hormones

The aim of this work was to study secretion and removal of insulin in hyperthyroidism. The experiments were carried out on two groups of male Wistar rats: control and hyperthyroid. Acute hyperthyyreosis was induced by administration of L-thyroxine (Fluka A.G.) 0.8 mg/kg for 21 days. Each group was divided into three subgroups: fed, fasted 24 h, fasted 24 h-treated with glucose. The insulin concentration was determined in the portal and aortal blood and a difference between the two concentrations was considered as reflecting insulin removal. The plasma insulin concentrations in both vessels of fed as well fasted hyperthyroid group were higher from the respective values in the control one. The removal of the hormone in the fed rats was similar in the both groups. Fasting reduced insulin removal only in the control group. Treatment of the fasted rats with glucose abolishes this difference. The liver glycogen content was similar in the two fasted groups but the blood glucose level was higher in the hyperthyroid than in the control rats. The latter factor could account for the difference in insulin removal between the two groups. It is concluded that hyperthyroidism increases insulin secretion but does not affect its removal.

Topics: Animals; Blood Glucose; Fasting; Glycogen; Hyperthyroidism; Insulin; Liver; Male; Rats; Rats, Inbred Strains; Thyroid Hormones

1. The effects of hyperthyroidism on the sensitivity and responsiveness of glycolysis and glycogen synthesis to insulin were investigated in the isolated incubated soleus muscle of the rat. 2. Hyperthyroidism, which was induced by administration of tri-iodothyronine (T3) to rats for 2, 5 or 10 days, increased fasting plasma concentrations of glucose, insulin and free fatty acids. 3. Administration of T3 for 2 or 5 days increased the rates of glycolysis at all insulin concentrations studied: this was due to increased rates of both glucose phosphorylation and glycogen breakdown, but there was no effect of T3 on the sensitivity of glycolysis to insulin. However, administration of T3 for 10 days increased the sensitivity of the rate of glycolysis to insulin. 4. The concentration of adenosine in the gastrocnemius muscles of the rats was not different from controls after 5 days, but it was markedly decreased after 10 days of T3 administration. If these changes are indicative of changes in the soleus muscle, the increased sensitivity of glycolysis to insulin found after 10 days' T3 administration could be due to the decrease in the concentration of adenosine. 5. Administration of T3 decreased the sensitivity of glycogen synthesis to insulin and the glycogen content of the soleus muscles. This may explain the decreased rates of non-oxidative glucose disposal found in spontaneous and experimental hyperthyroidism in man. 6. The rates of glucose oxidation did not change after 2 days, but they were increased after 5 and 10 days of T3 administration.

Topics: Adenosine; Animals; Fatty Acids, Nonesterified; Glucose; Glycogen; Glycolysis; Hexosephosphates; Hyperthyroidism; Insulin; Lactates; Lactic Acid; Male; Muscles; Phosphorylation; Rats; Rats, Inbred Strains; Triiodothyronine

Isolated hepatocytes from hyperthyroid and euthyroid rats showed the same rate and extent of activation of glycogen synthase after addition of glucose (10 mM or 60 mM). In liver cells from hypothyroid rats this activation occurred at a 7-fold lower rate. However, complete activation of glycogen synthase occurred eventually in broken-cell preparations from either source during incubation in vitro. Glycogen synthase phosphatase was then quantitatively assayed in liver homogenates with exogenous synthase b as substrate. These assays revealed an increased synthase phosphatase activity (approximately 160%) in the hyperthyroid liver and a decreased activity (to approximately 60%) in the livers from hypothyroid rats. These activity changes involved both the cytosolic and the glycogen-bound synthase phosphatase. The increase in the activity of synthase phosphatase after the administration of T3 became maximal after 48 h. We conclude that thyroid hormones control hepatic glycogen synthesis, at least partly by an effect on synthase phosphatase.

Topics: Animals; Enzyme Activation; Glucose; Glycogen; Glycogen Synthase; Glycogen-Synthase-D Phosphatase; Hyperthyroidism; Hypothyroidism; Liver; Male; Phosphorylase a; Rats; Rats, Inbred Strains; Triiodothyronine

A method is presented which allows simultaneous estimation of rates of glycogen synthesis and glycogenolysis in an isolated incubated skeletal muscle, thus allowing measurement of the glycogen/glucose-1-phosphate substrate cycling rate. In the absence of hormonal additions, the measured rates of glycogen synthesis and breakdown were similar [respectively, 0.54 +/- 0.12 (8) and 0.74 +/- 0.10 (8) mumol glucosyl equiv. h-1 (g tissue)-1]. Incremental addition of insulin stimulated glycogen synthesis up to threefold and reduced glycogenolysis by about sevenfold; the half-maximally effective concentration of insulin on both processes was about 100 microU/ml (0.7 nM). Incremental addition of adrenaline (in the presence of 1 mU insulin/ml) caused a dramatic increase in the glycogenolytic rate (about 15-fold), but a much less marked inhibition of glycogen synthetic rate. In addition to hormonal manipulation of the muscle preparation in vitro, the effects of cold exposure, the hyperthyroid state, a single exercise bout and exercise-training of animals in vivo on the rates of glycogen synthesis and breakdown in the isolated incubated muscle preparation have been investigated. Significant changes in measured glycogen synthesis, breakdown and glycogen/glucose-1-phosphate cycling have been observed, both under basal conditions and in response to hormonal additions in vitro. The results are discussed with respect to the possible physiological importance of this substrate cycle.

Topics: Adaptation, Physiological; Animals; Cold Temperature; Epinephrine; Glucosephosphates; Glycogen; Hyperthyroidism; Insulin; Male; Models, Biological; Muscles; Physical Exertion; Rats; Rats, Inbred Strains; Starvation

Seven hyperthyroid patients were studied by repeated muscle biopsies (vastus lateralis) before and after a period of medical treatment which averaged 10 months. The biopsies were analysed with regard to fibre-type composition, fibre area, capillary density, glycogen content and enzyme activities representing the glycolytic capacity (hexokinase, 6-phosphofructokinase), oxidative capacity (oxoglutarate dehydrogenase, citrate synthase) and Ca2+- and Mg2+-stimulated ATPase in muscle. In the pretreatment biopsy (hyperthyroid state), there was a significantly lower proportion of type I fibres (30% vs. 41%), a higher capillary density (23%), lower glycogen content (33%), and higher hexokinase activity (32%) compared with the post-treatment biopsy. No significant changes in the activity of the remaining enzymes were observed. The present study indicates that hyperthyroidism induces a transformation from type I to type II fibres in human skeletal muscle. The increase in hexokinase activity probably reflects a higher glucose utilization by skeletal muscle in order to compensate partially for the reduced glycogen content.

Topics: Adult; Biopsy; Ca(2+) Mg(2+)-ATPase; Calcium-Transporting ATPases; Citrate (si)-Synthase; Female; Glycogen; Hexokinase; Humans; Hyperthyroidism; Ketoglutarate Dehydrogenase Complex; Male; Methimazole; Middle Aged; Muscles; Phosphofructokinase-1; Thiouracil

We investigated the effect of hyperthyroidism and hypothyroidism on the myocardial glycogen metabolism by quantitating 125I-insulin binding, glycogen content, glycogen synthase and phosphorylase enzyme activities in the newborn rabbit. Although an increase in 125I-insulin binding was observed in response to hyperthyroidism (p less than 0.01), a decrease in myocardial glycogen (p less than 0.01) along with no change in the synthase and phosphorylase enzyme activity was demonstrated. On the other hand, propylthiouracil-induced hypothyroxinemia did not affect the 125I-insulin binding, glycogen content or the two enzyme systems. We conclude that the depletion of myocardial glycogen secondary to hyperthyroidism is independent of an increase in 125I-insulin binding or any change in the major glycogen enzyme activities (synthase and phosphorylase). We speculate that this decline in neonatal heart glycogen may be secondary to thyroxine-induced altered glucose uptake or modified postinsulin receptor events.

Topics: Animals; Animals, Newborn; Blood Glucose; Congenital Hypothyroidism; Female; Fetal Diseases; Glycogen; Hyperthyroidism; Hypothyroidism; Insulin; Myocardium; Pregnancy; Rabbits; Thyroid Hormones; Thyroxine

Glucose metabolism was studied as evidenced by the sugar and pyruvic acid levels in blood and glycogen and pyruvic acid content of tissues in euthyroid, hypothyroid and hyperthyroid rats by giving insulin. Results show that in a normal thyroxine-excess insulin state, the rise in blood sugar was less, glycogenesis was much enhanced and glycolysis was reduced in comparison to these data in the euthyroid state. When tyroxine deficiency was associated with excess insulin, glycogenesis was enhanced further and an almost complete inhibition of glycolysis was observed. In excess thyroxine-excess insulin state glycogenesis was increased at the expense of glycolysis in comparison to the finding in the hyperthyroid state. Thus exogenous insulin in the euthyroid state altered the pattern of carbohydrate metabolism enhancing glycogenesis and inhibiting glycolysis. In a low thyroxine-excess insulin state, further enhancement of glycogenesis and inhibition of glycolysis were observed. But in an excess thyroxine-excess insulin state, the higher thyroxine activity was somewhat neutralized by higher insulin action allowing glycogenesis with glucose to proceed to some extent.

Topics: Animals; Blood Glucose; Female; Glucose; Glycogen; Hyperthyroidism; Hypothyroidism; Insulin; Kidney; Liver; Liver Glycogen; Male; Myocardium; Pyruvates; Pyruvic Acid; Rats; Rats, Inbred Strains; Thyroxine

The actions of hormones which are associated to cAMP-dependent and calcium-dependent mechanisms of signal transduction were studied in hepatocytes obtained from rats with different thyroid states. In cells from euthyroid and hyperthyroid rats, the metabolic actions of epinephrine were mediated mainly through alpha 1-adrenoceptors; beta-adrenoceptors seem to be functionally unimportant. In contrast, both alpha 1- and beta-adrenoceptors mediate the actions of epinephrine in hepatocytes from hypothyroid animals. Phosphatidylinositol labeling was strongly stimulated by epinephrine, vasopressin and angiotensin II in cells from eu-, hyper- or hypothyroid rats. However, metabolic responsiveness to vasopressin and angiotensin II was markedly impaired in the hypothyroid state. The glycogenolytic response to the calcium ionophore A-23187 was also impaired, suggesting that hepatocytes from hypothyroid rats are less sensitive to calcium signalling. The persistence of alpha 1-adrenergic responsiveness in the hypothyroid state suggests that the mechanism of signal transduction for alpha 1-adrenergic amines is not identical to that of the vasopressor peptides. alpha 1-Adrenergic stimulation of cyclic AMP accumulation was not detected in cells from hypothyroid rats. These data suggest that factors besides calcium and besides cAMP are probably involved in alpha 1-adrenergic actions. Metabolic responses to glucagon and to the cAMP analogue dibutyryl cAMP were not markedly changed during hypothyroidism, although cAMP accumulation produced by glucagon and beta-adrenergic agonists was enhanced. In hyperthyroidism, cell responsiveness to epinephrine, vasopressin, angiotensin II and glucagon was decreased, but sensitivity to cAMP was not markedly altered. The factors involved in this hyposensitivity to hormones during hyperthyroidism are unclear.

Topics: Angiotensin II; Animals; Calcium; Cyclic AMP; Gluconeogenesis; Glycogen; Hyperthyroidism; Hypothyroidism; Liver; Liver Glycogen; Phosphatidylinositols; Rats; Receptors, Adrenergic, alpha; Urea; Vasopressins

Topics: Acid Phosphatase; Adult; Female; Glucuronidase; Glycogen; Humans; Hyperthyroidism; Hypothyroidism; In Vitro Techniques; Leukocyte Count; Male; Middle Aged; Neutrophils; Oxidation-Reduction; Oxidoreductases; Phagocytosis

The postnatal development of the neurons of the cuneate nucleus was examined ultrastructurally in euthyroid and hypothyroid rats from birth to the sixth postnatal week. In the euthyroid animals, the neurons at birth displayed mild nuclear invaginations and a scanty cytoplasm with few organelles. By 2 weeks, there was a considerable increase in Nissl bodies. At 3 weeks, the neurons contained short lamellar arrays of endoplasmic reticulum. Between 3 and 6 weeks there was a reduction in the Nissl substance. In the hypothyroid animals, although the sequence of maturational changes generally resembled that of the controls, a number of differences were noted. The neurons at 1 week displayed dilations of perinuclear space, rough endoplasmic reticulum, Golgi complexes, and mitochondria. At 4 weeks both perikaryon and myelinated axons contained glycogen. Several neurons with cytoplasmic inclusions considered to be nonfunctional RNA were seen. The 6-week hypothyroid neuron exhibited large, clear, cytoplasmic vacuoles associated with a drastic reduction in cytoplasmic organelles. Presynaptic terminals showed a 50% reduction in mitochondrial numbers associated with the presence of glycogen granules. Three changes observed in neurites in all the age groups included: (1) large accumulation of glycogen in presynaptic terminals; (2) clear vacuoles; and (3) the presence of numerous lamellar bodies within reactive axons. Aberrant myelination, such as a single myelin sheath enclosing multiple processes, and instances of collapsed and redundant myelin were encountered.

Topics: Animals; Animals, Newborn; Endoplasmic Reticulum; Glycogen; Hyperthyroidism; Medulla Oblongata; Nerve Endings; Neurons; Nissl Bodies; Rats; Rats, Inbred Strains; Vacuoles

Changes induced in liver and striated muscle glycogen and glycogen enzymes (glycogen synthetase, glycogen phosphorylase and alpha-amylase) by hypothyroidism and hyperthyroidism in rats have been determined. There were no changes in liver glycogen synthetase, phosphorylase and amylase activities in the hypothyroid group. Hyperthyroid rats showed lower liver glycogen synthetase, phosphorylase a and amylase activities. In muscle, hypothyroid rats had lower phosphorylase activity. In the hyperthyroid group glycogen synthetase was increased.--The results presented do not completely agree with the glycogen levels found in both tissues studied, and they are obviously more related to other factors such as glucose availability. It can be concluded that under the conditions studied, the glycogen enzyme levels could not alone explain the variations of glycogen levels.

Topics: Amylases; Animals; Blood Glucose; Body Weight; Glycogen; Glycogen Synthase; Hyperthyroidism; Hypothyroidism; Liver; Liver Glycogen; Male; Muscles; Phosphorylases; Rats; Rats, Inbred Strains

Coronary arteries and arterioles in the left and right ventricles from normal and hyperthyroid rats were examined histochemically to determine and to compare their metabolic activities. The test animals were made hyperthyroid by administration of desiccated thyroid for 8-10 weeks. Using histochemical techniques, selected enzymes and components of key metabolic pathways were examined. These pathways included an evaluation of aerobic (oxidative phosphorylation, Kreb's cycle and respiratory chain) and anaerobic metabolic capacity, hexose-monophosphate shunt activity, amounts of deoxyribonucleic and ribonucleic acids present and activity of beta-oxidation of fatty acids. Our results indicate that normal coronary arteriolar metabolism is predominantly aerobic. The findings also suggest a reduction in aerobic metabolism with an accompanying increase in anaerobic potential in the hyperthyroid coronary arterioles. Thus, during thyrotoxicosis, the coronary arterioles may partially shift from aerobic to anaerobic metabolism. Moreover, in both the normal and thyrotoxic rat heart, the coronary microvasculature appears quite stable with little cell proliferation. In contrast, both the control and hyperthyroid rat coronary arteries appear to utilize primarily anaerobic pathways, while the control and hyperthyroid myocardium seem highly dependent upon aerobic metabolism. The tremendous reduction in glucose-6-phosphate dehydrogenase activity in hyperthyroid, when compared to normal coronary arteries and some larger arterioles, implies a reduced capacity for nucleic acid and protein synthesis in the test animals.

Topics: Animals; Coronary Vessels; Glycogen; Histocytochemistry; Hyperthyroidism; Male; Myocardium; Nucleic Acids; Rats; Rats, Inbred Strains

In the heart the interaction of the thyroid hormones, the catecholamines and the effect of the beta-blocker was studied. The binding of the radioactive noradrenalin (3H-NA) was higher in the particles of the thyreotoxic myocardium of the dog got by centrifugation at 1,000 and 78,000 g. The 3H-NA-binding was inhibited with propranolol, isoprenalin and in lower concentrations with trimepranol in dogs and also in rats. In the myocardium of the thyreotoxic dogs 3H-NA was less superseded with isoprenalin, in the myocardium of thyreotoxic rats less with non-active norarenalin in comparison to euthyroid animals. The thyreotoxicosis caused an increase of the activities of phosphorylase, of the lipases, of the calcium-dependent ATPase, the protein kinase in presence of histone, further a decrease of the activity of adenyl cyclase, particularly in presence of sodium fluoride and a decrease of the concentration of the cyclic adenosine monophosphate in the myocardium of the rats and dogs, respectively. The pharmacological thyreotoxicosis decreased the concentration of the heart glycogen. This decrease was inhibited by the beta-blocker trimepranol, but not by the alpha-blocker phentolamine. Three possibilities of the explanation of the findings of this complex study are cited. The influence of the thyroid hormones and beta-blockers 1. on the transport and calcium metabolism, 2. on the synthesis of the heart proteins, 3. on the backbinding control of the hormonal effect at cellular level.

Topics: Animals; Calcium-Transporting ATPases; Cyclic AMP; Dogs; Glycogen; Hyperthyroidism; Isoproterenol; Lipase; Male; Metipranolol; Myocardium; Norepinephrine; Phentolamine; Phosphorylases; Propranolol; Rats; Receptors, Adrenergic; Receptors, Adrenergic, beta

Topics: Adenosine Triphosphate; Adenylyl Cyclases; Animals; Cyclic AMP; Dogs; Glycogen; Hyperthyroidism; Lipase; Myocardium; Phosphorylases; Protein Kinases; Rats; Receptors, Adrenergic

Topics: Adenosine Triphosphate; Animals; Creatine; Creatine Kinase; Glycogen; Hyperthyroidism; Hypothyroidism; Muscles; Phosphocreatine; Rats

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; DNA; Electron Transport Complex IV; Female; Glycogen; Histocytochemistry; Humans; Hyperthyroidism; Leukocytes; Lipids; Male; Middle Aged; Neutrophils; Peroxidases; Succinate Dehydrogenase

Morphological and electrophysiological studies were performed on intercostal muscle biopsies from 2 thyrotoxic patients. The diseased fibers had numerous areas of subsarcolemmal glyogen accumulations and abnormal membranous projections. Both Type I and Type II muscle fibers were atrophied. Diseased fibers were substantially depolarized and when artifically hyperpolarized showed earlier inactivation of the sodium conductance as a function of membrane potential, and a critical depolarization potential more depolarized than in normal fibers. When stimulated at 20 pulses/sec, or faster, the diseased fibers could not generate normal action potentials due to membrane depolarization and the appearance of a marked after-hyperpolarization. Muscle weakness associated with hyperthyroidism is attributed to the reduced membrane excitability.

Topics: Adult; Electric Stimulation; Electrophysiology; Female; Glycogen; Histocytochemistry; Humans; Hyperthyroidism; In Vitro Techniques; Intercostal Muscles; Male; Membrane Potentials; Microscopy, Electron

Topics: Amoxicillin; Ampicillin; Animals; Cephalexin; Glycogen; Hyperthyroidism; Lethal Dose 50; Lipid Metabolism; Male; Methacycline; Phospholipids; Rats

Topics: Animals; Glycogen; Golgi Apparatus; Heart Failure; Histocytochemistry; Hyperthyroidism; Lipids; Lysosomes; Male; Mitochondria, Muscle; Myocardium; Myofibrils; Oxygen Consumption; Papillary Muscles; Rats; Sarcoplasmic Reticulum; Thyroid Function Tests

Topics: Adenosine Triphosphate; Amino Acids; Animals; Body Weight; Brain; Brain Chemistry; Carbon Dioxide; Carbon Radioisotopes; Glucose; Glycogen; Hyperthyroidism; Hypothyroidism; Leucine; Lipids; Liver; Organ Size; Phosphocreatine; Rats; Time Factors

Topics: Adenosine Triphosphatases; Adenylyl Cyclases; Adult; Calcium; Cyclic AMP; Cytochrome c Group; Electrophoresis, Polyacrylamide Gel; Glucosyltransferases; Glycogen; Hexokinase; Histocytochemistry; Humans; Hyperthyroidism; Magnesium; Male; Muscles; Oxidoreductases; Paralyses, Familial Periodic; Phosphofructokinase-1; Sarcoplasmic Reticulum

Topics: Adult; Animals; Blood Glucose; Blood Pressure; Dogs; Fatty Acids, Nonesterified; Glycogen; Heart Rate; Hemodynamics; Humans; Hyperthyroidism; Lactates; Liver Glycogen; Male; Metabolism; Middle Aged; Muscles; Oxygen Consumption; Physical Exertion; Propranolol; Pyruvates; Rats; Receptors, Adrenergic; Triglycerides

Topics: Acyltransferases; Adolescent; Adult; Alkaline Phosphatase; Anemia, Hemolytic; Biliary Tract Diseases; Child; Child, Preschool; Cystic Fibrosis; Erythroblastosis, Fetal; Female; gamma-Glutamyltransferase; Glutamate Dehydrogenase; Glycogen; Hematologic Diseases; Hepatitis A; Humans; Hyperthyroidism; Hypothyroidism; Infant; Infant, Newborn; Kidney Diseases; Leucyl Aminopeptidase; Neoplasms; Oxidoreductases; Pregnancy

Topics: Adult; Biopsy; Cell Membrane; Endoplasmic Reticulum; Glycogen; Golgi Apparatus; Histocytochemistry; Humans; Hyperthyroidism; Male; Microscopy, Electron; Mitochondria; Muscles; Myofibrils; Paralysis; Periodicity

Topics: Adult; Glycogen; Humans; Hyperthyroidism; Male; Microscopy, Electron; Mitochondria, Muscle; Mitochondrial Swelling; Muscles; Paralysis

Topics: Animals; Creatine; Female; Glycogen; Hyperthyroidism; Male; Muscles; Myocardium; Rats; Thyroid Hormones

Topics: Adrenocorticotropic Hormone; Animals; Beriberi; Fasting; Fatty Acids, Nonesterified; Glucose; Glycogen; Hyperthyroidism; Lipoprotein Lipase; Male; Myocardium; Oxidative Phosphorylation; Rats

Topics: Adenine Nucleotides; Adenosine Triphosphate; Animals; Chromatography; Glycogen; Hyperthyroidism; Lactates; Male; Methods; Myocardium; Rabbits

Topics: Cell Nucleus; Chronic Disease; Diagnosis, Differential; Glycogen; Histocytochemistry; Humans; Hyperthyroidism; Hypokalemia; Lysosomes; Male; Methods; Microscopy; Microscopy, Electron; Middle Aged; Muscles; Myofibrils; Paralyses, Familial Periodic; Paralysis; Sarcolemma

Topics: Animals; Antithyroid Agents; Cholesterol; Depression, Chemical; Dietary Proteins; Glutamates; Glycogen; Hyperthyroidism; Iodine; Iodine Radioisotopes; Liver Glycogen; Muscles; Oxygen Consumption; Protein Deficiency; Rats; Stimulation, Chemical; Thyroid Function Tests; Thyroid Gland

Topics: Adrenal Glands; Animals; Cardiovascular Physiological Phenomena; Catecholamines; Epinephrine; Glucosyltransferases; Glycogen; Heart Rate; Hyperthyroidism; Injections, Intraperitoneal; Kidney; Liver; Male; Myocardium; Norepinephrine; Oxygen Consumption; Phentolamine; Propranolol; Rats; Reserpine; Spleen; Thyroxine

Topics: Adult; Biopsy; Cell Membrane; Endoplasmic Reticulum; Glycogen; Humans; Hyperthyroidism; Hypokalemia; Male; Microscopy, Electron; Muscles; Paralysis

Topics: Animals; Cardiomyopathies; Glycogen; Hyperthyroidism; Magnesium; Methionine; Myocardium; Phosphocreatine; Rabbits

Topics: Antithyroid Agents; Creatine Kinase; Fructose; Glucose; Glycogen; Humans; Hyperthyroidism; In Vitro Techniques; Ischemia; Lactates; Male; Middle Aged; Muscle Cramp; Muscles; Propylthiouracil

Topics: Animals; Cartilage, Articular; Endoplasmic Reticulum; Glycogen; Hyperthyroidism; Male; Mice; Microscopy, Electron; Mitochondria; Ribosomes; Thyroxine

Topics: Adult; Anemia, Hemolytic; Cardiovascular Diseases; Chronic Disease; Diabetes Mellitus; Female; Gastrointestinal Diseases; Gestational Age; Glycogen; Humans; Hyperthyroidism; Infant, Newborn; Liver Diseases; Neoplasms; Nephritis, Interstitial; Postpartum Period; Pregnancy; Respiratory Tract Diseases

Topics: Animals; Creatine; Female; Glycogen; Hyperthyroidism; Male; Muscles; Phosphorus; Potassium; Rats; Thyrotropin; Thyroxine

Topics: Animals; Biopsy; Dogs; Glycogen; Hyperthyroidism; Lipid Metabolism; Male; Microscopy, Electron; Muscles; Oxygen Consumption

Topics: Adrenal Glands; Animals; Blood Cell Count; Cardiomegaly; Cardiovascular System; Catecholamines; Electrocardiography; Epinephrine; Glycogen; Heart; Hemoglobins; Hyperthyroidism; Hypertrophy; Myocardium; Nitrogen; Norepinephrine; Organ Size; Protein Biosynthesis; Rabbits; Thyroid Hormones; Water-Electrolyte Balance

Topics: Adenocarcinoma, Papillary; Adult; Culture Techniques; Cytoplasm; DNA; Female; Glycogen; Goiter; Humans; Hyperthyroidism; Iodine Isotopes; Microscopy, Fluorescence; Microscopy, Phase-Contrast; Middle Aged; Motion Pictures; Oncogenic Viruses; Thyroid Gland; Thyroid Neoplasms

Topics: Animals; Blood; Blood Proteins; Creatine; Diiodotyrosine; Enzymes; Glycogen; Hyperthyroidism; In Vitro Techniques; Iodine; Liver; Liver Glycogen; Muscles; Peroxidases; Rabbits; Stress, Physiological; Tyrosine

Topics: Animals; Arabinose; Carbohydrate Metabolism; Diabetes Mellitus, Experimental; Diaphragm; Electric Stimulation; Glucose; Glycogen; Hyperthyroidism; In Vitro Techniques; Insulin; Mannose; Muscle Contraction; Muscle, Smooth; Muscles; Myocardium; Rats; Research; Sucrose; Xylose

Topics: Acetohexamide; Blood Chemical Analysis; Blood Glucose; Carbohydrate Metabolism; Epinephrine; Glucose Tolerance Test; Glycogen; Hydrocortisone; Hyperthyroidism; Insulin; Islets of Langerhans; Pharmacology; Phosphorus; Thyroid Hormones; Tolbutamide

Topics: Carbohydrate Metabolism; Female; Glycogen; Guinea Pigs; Histological Techniques; Hyperthyroidism; Lipid Metabolism; Pathology; Placenta; Pregnancy; Pregnancy, Animal; Research; Thyroxine; Toxicology

Topics: Animals; Electron Transport Complex II; Glycogen; Hyperthyroidism; Myocardium; Rabbits; Succinate Dehydrogenase; Thyroxine

Topics: Adenine Nucleotides; Glycogen; Glycogenolysis; Hyperthyroidism; Liver; Nucleosides; Nucleotides

Topics: Blood Glucose; Epinephrine; Glycogen; Glycogenolysis; Humans; Hyperthyroidism

Topics: Diaphragm; Glycogen; Glycogenolysis; Hyperthyroidism; Insulin; Insulins

Topics: Glycogen; Glycogenolysis; Hyperthyroidism; Liver

Topics: Animals; Folic Acid; Glycogen; Hyperthyroidism; Liver; Rats; Thyroid Gland; Vitamin B Complex; Vitamins