Thyroid hormone increasing

Basal metabolic rate is decreased under conditions of starvation (including dieting as noted above one more reason why it is tough to lose weight) and increased under conditions of feeding. These responses tend to keep body weight constant. Thyroid hormone increases basal metabolic rate. Hyperthyroid people tend to be slender. 

The mechanisms by which thyroid hormones enhance antidepressant activity are still unknown. It is of interest that thyroid hormone increases net activity of several neurotransmitters that are putatively involved in the pathophysiology of depression in a way that is descriptively similar to that of estrogens. Receptors for the two hormones belong to the same superfamily. As was previously mentioned [Pfaff 1996], these issues are currently being explored, and clarifications are expected shortly. 

Experimental studies have documented changes in drug response caused by increases or decreases in the number of receptor sites or by alterations in the efficiency of coupling of receptors to distal effector mechanisms. In some cases, the change in receptor number is caused by other hormones for example, thyroid hormones increase both the number of 3 receptors in rat heart muscle and cardiac sensitivity to catecholamines. Similar changes probably contribute to the tachycardia of thyrotoxicosis in patients and may account for the usefulness of propranolol, a 3-adrenoceptor antagonist, in ameliorating symptoms of this disease. 

Even a single dose of corticotropin can cause inhibition of thyrotrophic hormone secretion (19), although the effect is brief. Conversely, thyroid hormones increase the sensitivity of adrenocortical cells in vitro to corticotropin (20) and hyperthyroidism increases sensitivity to corticotropin (21,22). 

Bogazzi F, Bartalena L, Campomori A, Brogioni S, Traino C, De Martino F, Rossi G, Lippi F, Pinchera A, Martino E. Treatment with lithium prevents serum thyroid hormone increase after thionamide withdrawal and radioiodine therapy in patients with Graves disease. J Clin Endocrinol Metab 2002 87(10) 4490-5. 

Cardiovascular Effects. Thyroid hormones appear to increase heart rate and myocardial contractility, thus leading to an increase in cardiac output. It is unclear, however, if this occurrence is a direct effect of these hormones or if the thyroid hormones increase myocardial sensitivity to other hormones (norepinephrine and epinephrine). 

Thyroid hormones Increased therapeutic and possibly toxic effects of both drugs CNS stimulation ... 

As in insects, a complex interaction of hormones in the amphibian larva precipitates metamorphosis. Ultimately, two major classes of hormones act together to control amphibian metamorphosis the thyroid hormones (made by the thyroid gland) and prolactin (made by the pituitary gland). Thyroid hormones function somewhat like the molting hormones of insects, in that an increase of their concentration relative to prolactin leads to metamorphosis of the larva into the adult. Prolactin functions somewhat like the juvenile hormones of insects, in that it tempers the action of the thyroid hormones. In most species, thyroid hormones increase dramatically in concentration during metamorphosis and this stimulates resorption of certain larval organs and differentiation of new adult organs. 

Thyroid hormone has multiple effects on the cardiovascular system with various physiological consequences. Several genes that encode important regulatory and structural proteins in the heart have been shown to be thyroid hormone responsive. Thyroid hormone increases cardiac contractility, induces vasorelaxation and angiogenesis, prevents fibrosis and has favorable effects on lipid metabolism (reviewed by Pantos73). 

Sun, Z.-Q., Ojamaa, K., Nakamura, T.Y., Artman, M., Klein, I. and Coetzee, W. (2001) A thyroid hormone increases pacemaker activity in rat neonatal atrial myocytes. Journal of Molecular and Cellular Cardiology, 33, 811-824. 

Treatment with thyroid hormone increases and thyroidectomy decreases cholesterol 7a-hydroxylase activity as well as HMG-CoA reductase activity [75,234,235]. As shown by Balasubramaniam et al. treatment with thyroid hormone increases first the cholesterol 7a-hydroxylase activity and then, after a time lag of several hours, HMG-CoA reductase [234]. Thus, it is likely that the rise in HMG-CoA reductase activity in this case is secondary to the depletion of cholesterol by cholesterol 7a-hydroxylase. 

Thyroid hormone increases the catabolism of clotting factors, resulting in an increased rate of synthesis of active clotting factors (recall that the function of vitamin K is primarily in reactivation). 

In addition to increased transcription of genes encoding TCA cycle enzymes and certain other enzymes of fuel oxidation, thyroid hormones increase the level of UCP2 and UCP3. In hyperthyroidism, the efficiency with which energy is derived from the oxidation of these fuels is significantly less than normal. As a consequence of the increased rate of the electron transport chain, hyperthyroidism results in increased heat production. Patients with hyperthyroidism, such as X.S. Teefore, complain of constantly feeling hot and sweaty. 

Thyroid hormone increases the sensitivity of the (3 cells of the pancreas to those stimuli that normally promote insulin release and is required for optimal insulin secretion. 

Thyroid hormone increases glomerular filtration rate. The answer is (B). 

Thyroid hormones increase the oxygen consumption of most isolated tissues but not of isolated adult brain. This suggests that the behavioral changes seen in abnormal thyroid states (anxiety and nervousness in hyperthyroidism and impaired memory in hypothyroidism) in the adult are not directly linked to overall changes in brain oxygen consumption. 

Oral anticoagulants—Thyroid hormones increase catabolism of vitamin K-dependent clotting factors. 

The thyroid hormone increases basal metabolic rate (resting energy expenditure). It has both direct actions and indirect effects on the metabolism by modifying the activities of other hormones such as catecholamines. The thyroid hormone also promotes growth. The thyroid hormone s action on metabolism is dose dependent. 

In general, the thyroid hormone increases glucose level by glycogenolysis and gluconeogenesis, stimulates lipolysis especially in hyperthyroidism. In normal conditions, the thyroid hormone has stimulatory effects on the synthesis of proteins but also leads to catabolic reactions in muscle under hypo- and hyperthyroid states [10]. 

Ohe conclusions suggested by the kinetic data obtained few years ago were that 1) the microtubule polymerization activity increases during brain development. This evolution seems to be related to the differential expxression of the microtubule-associated proteins, such as Tau proteins, differing in size and in polymerization activity 2) thyroid hormones increase the polymerization activity probably because they accelerate the transition fron the inmature to the more active mature Tau forms. However, little was knewn on the mechanism that generates Tau heterogeneity at different stages of brain development, and on the site of action of thyroid hormones. 

It was mentioned that the administration of thyroid hormones increases the activity of NADPH cytochrome c reductase, a process that accelerates NADPH oxidation through a pathway not coupled with phosphorylation. 

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