Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Metabolic rate thyroid hormone effect

Wada, L., and King, J- C, (1986), Effect of low zinc intakes on basal metabolic rate, thyroid hormones, and protein utilization in adult men / Niiir. 116, 1045-1053. [Pg.871]

Thyroid hormone effects on metabolism arc diverse. The rates of protein and carbohydrate synthesis and catabolism are inlluenced. An example of the effect of thyroid hormones on lipid metabolism is the observation of a high serum cholesterol in some hypothyroid patients. This is a consequence of a reduction in cholesterol metabolism due to down regulation of low-density lipoprotein (LDL) receptors on liver cell membranes, with a subsequent failure of sterol excretion via the gut. [Pg.144]

Metabolic Functions. The functions of the thyroid hormones and thus of iodine are control of energy transductions (121). These hormones increase oxygen consumption and basal metaboHc rate by accelerating reactions in nearly all cells of the body. A part of this effect is attributed to increase in activity of many enzymes. Additionally, protein synthesis is affected by the thyroid hormones (121,122). [Pg.386]

Triiodothyronine (3, 5,3-L-triiodothyronine, T3) is a thyroid hormone. It is producedby outer ring deiodination of thyroxine (T4) in peripheral tissues. The biologic activity of T3 is 3-8 times higher than that of T4. T3 is 99.7% protein-bound and is effective in its free non-protein-bound form. The half-life of triiodothyronine is about 19 h. The daily tur nover of T3 is 75%. Triiodothyronine acts via nuclear receptor binding with subsequent induction of protein synthesis. Effects of thyroid hormones are apparent in almost all organ systems. They include effects on the basal metabolic rate and the metabolisms of proteins, lipids and carbohydrates. [Pg.1243]

Demonstration that the effects of thyrotoxicosis or goiter are due to an excess or deficiency in (thyroxine + T3) secretion does not explain how the diseases originate nor why development and metabolic rate are affected. It is thought that some cases of thyrotoxicosis (Graves disease) may be caused by abnormal immune responses mimicking the effects of thyroid-stimulating hormone on the thyroid gland. [Pg.40]

Z)-2,3-Methanothyronine 59 and its dibromo derivative 60 have comparable activity with the thyroxine 61, a thyroid hormone [66], which exhibited thyro-mimetic activities in basal metabolism and antigoiter tests (comparison of oxygen consumption and heart rate in normal and thyroidectomized rats) but did not have an inhibitory action on the metabolism developed by triiodothyronine [66]. (Z)-2,3-Methanohistidine 62, tested on rat liver, is an effective inhibitor of histidine decarboxylase, Eq. (23) [67]. [Pg.14]

In patients with longstanding hypothyroidism and those with ischemic heart disease, rapid correction of hypothyroidism may precipitate angina, cardiac arrhythmias, or other adverse effects. For these patients, replacement therapy should be started at low initial doses, followed by slow titration to full replacement as tolerated over several months. If hypothyroidism and some degree of adrenal insufficiency coexist, an appropriate adjustment of the corticosteroid replacement must be initiated prior to thyroid hormone replacement therapy. This prevents acute adrenocortical insufficiency that could otherwise arise from a thyroid hormone-induced increase in the metabolic clearance rate of adrenocortical hormones. [Pg.748]

Mechanism of Action A synthetic form of triiodothyronine (T3), a thyroid hormone involved in normal metabolism, growth, and development. Possesses catabolic and anabolic effects. Therapeutic Effect Increases basal metabolic rate, enhances gluco-neogenesis, and stimulates protein synthesis. [Pg.701]

Thyroid hormones are intimately involved in regulating the basal metabolic rate. Liver tissue of animals given excess thyroxine shows an increased rate of 02 consumption and increased heat output (thermogenesis), but the ATP concentration in the tissue is normal. Different explanations have been offered for the thermogenic effect of thyroxine. One is that excess thryroxine causes uncoupling of oxidative phosphorylation in mitochondria. How could such an effect account for the observations Another explanation suggests that the thermogenesis is due to an increased rate of ATP utilization by the thyroxine-stimulated tissue. Is this a reasonable explanation Why ... [Pg.919]

Thyroxine and triiodothyronine have many effects, a major one in mammals and birds being stimulation of energy metabolism in tissues. It has long been recognized that a deficiency of thyroid hormone is reflected in an overall lower basal metabolic rate (Chapter 6). Maley and Lardy observed that thyroxine uncouples oxidative phosphorylation (Chapter 18) in isolated mitochondria.117 When mitochondria from animals receiving extra thyroxine were compared with those from control animals, an increased rate of electron transport was observed. However, there was little or no change in the P / O ratio. Thus, the hormone apparently increased the rate of electron transport... [Pg.1432]

Most readers would assume that the low percentage of T-4 and T-3 provided by Armour was ineffective. In fact, the combination was often considered more effective than either drug alone and is at the correct human ratio. The trace levels of T-2 and Triacana create a complete synergystic and effective thyroid hormone drug. Most athletes realized an increased metabolic rate with only 1.5-2.0 grains daily. [Pg.110]

It has been suggested that thyroid status is a possible major regulator of metabolic rate. Herlihy et al. [38] found that CR reduces the 24-hour mean serum triiodothyronine (T3) level, but not the thyroxine (T4) level. CR appears to have this action because it attenuates the circadian amplitude in the concentrations of both hormones. However, Snyder et al. [39] found no effect of CR on either T4 or T3 in young rats and no consistent effect of CR on age-related changes in the concentrations of these two hormones. [Pg.219]

Differences in enantiomers become apparent in their interactions with other chiral molecules, such as enzymes. Still, we need a simple method to distinguish between enantiomers and measure their purity in the laboratory. Polarimetry is a common method used to distinguish between enantiomers, based on their ability to rotate the plane of polarized light in opposite directions. For example, the two enantiomers of thyroid hormone are shown below. The (5) enantiomer has a powerful effect on the metabolic rate of all the cells in the body. The (R) enantiomer is useless. In the laboratory, we distinguish between the enantiomers by observing that the active one rotates the plane of polarized light to the left. [Pg.185]

Q3 The thyroid hormones thyroxine and triiodothyronine have many metabolic effects. In adults they increase metabolic rate, oxygen and calorie consumption, stimulate carbohydrate metabolism and turnover of protein, deplete fat stores and increase catabolism of free fatty acids. Thyroid hormones stimulate heart rate and force and increase pulmonary ventilation, gastrointestinal motility and central nervous system (CNS) activity. Actions on the heart can result in an increased incidence of dysrhythmias. Thyroid hormones are critical for the normal growth and development of the infant, particularly in respect of skeletal growth and maturation of the CNS. [Pg.146]

Adverse effects of thyroid hormone parallel the increase in metabolic rate. The symptoms and signs are those of hyperthyroidism. Symptoms of myocardial ischaemia, atrial fibrillation or heart failure are liable to be provoked by too vigorous therapy or in patients having serious ischaemic heart disease who may even be unable to tolerate optimal therapy. Should they occur levothyroxine must be discontinued for at least a week and begim again at lower dosage. Only slight overdose is needed to precipitate atrial fibrillation in patients over 60 years. [Pg.701]

Quick relief can be obtained with a p-adrenoceptor blocking drug (judge dose by heart rate) though these do not block all the metabolic effects of the hormone, e.g. on the myocardium, and the basal metabolic rate is unchanged. For this reason they should not be used as sole therapy except in mild thyrotoxicosis in preparation for radioiodine treatment, and should be continued in these patients until the radioiodine has taken effect. They do not alter the course of the disease, nor biochemical tests of thyroid function. Any effect on thyroid hormonal action on peripheral tissues is clinically unimportant. It is desirable to choose a drug that is nonselective for pj and p2 receptors and lacks partial agonist effect (e.g. propranolol 20-80 mg 6-8-hourly, or timolol 5 mg once daily). Usual contraindications to P-blockade (see p. 478) should be observed, especially asthma. [Pg.703]

In patients with hypothyroidism, the stimulatory effect of thyroid hormone on the oxidation of fuels is diminished. As a consequence, the generation of ATP is reduced, causing a sense of weakness, fatigue, and hypokinesis. The reduced metabolic rate is associated with diminished heat production, causing cold intolerance and decreased sweating. With less demand for the delivery of fuels and oxygen to peripheral tissues, the circulation is slowed, causing a reduction in heart rate and, when far advanced, a reduction in blood pressure. [Pg.292]

Thyroid hormones are necessary for metabolism, growth, and development. The main effect of thyroid hormones is increased metabolic rate, increased oxygen consumption, and increased metabolism of carbohydrates. Because the mixture contains both T3 and T4, systemic toxicity will be evident within a few hours and may be quite prolonged. Synthetic products that contain only T4 can have a latent period of several days before the development of significant symptoms. [Pg.2577]

Thyroid hormones have many important biological effects. A major function is their control of the basal metabolic rate and calorigenesis through increased oxygen consumption in tissue via the effects of thyroid hormone on membrane... [Pg.2054]

Hypersecretion of thyroid hormone (thyrotoxicosis) occurs in Graves s disease due to autoimmune stimulation of the thyroid gland mimicking the effects of TSH. Symptoms are high metabolic rate, increased temperature and sweating, nervousness, tremor, tachycardia, increased appetite and loss of weight, goitre and protrusion of the eyeballs (exophthalmia). [Pg.103]


See other pages where Metabolic rate thyroid hormone effect is mentioned: [Pg.66]    [Pg.337]    [Pg.745]    [Pg.118]    [Pg.174]    [Pg.96]    [Pg.47]    [Pg.218]    [Pg.3413]    [Pg.36]    [Pg.329]    [Pg.2055]    [Pg.315]    [Pg.224]    [Pg.127]    [Pg.71]    [Pg.44]    [Pg.150]    [Pg.407]    [Pg.318]    [Pg.66]    [Pg.415]    [Pg.416]    [Pg.408]    [Pg.75]    [Pg.539]   
See also in sourсe #XX -- [ Pg.3 , Pg.570 ]




SEARCH



Hormonal effects

Hormone metabolism

Hormones metabolic

Hormones metabolic effects

Metabolic effects

Metabolism effects

Metabolism rates

Thyroid hormone hormonal effects

Thyroid hormones

Thyroid hormones metabolism

Thyroidal hormone

© 2024 chempedia.info