Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is suggested that in addition to stimulating the thyroid gland (i.e., the main regulator of metabolic-rate in adults) thyroid-stimulating hormone (T.S.H.) stimulates the second thermoregulatory organ (i.e., the brown adipose tissue). Brown fat functions as a thermogenic organ in hibernating animals, in newborn infants, and during cold acclimatisation. However, B.F. may persist in childhood and in some adults. Its hypertrophy in response to T.S.H. could account for certain unexplained features of myxoedema in which serum-T.S.H. is raised, such as swelling of the supraclavicular fat pad and the less commonly encountered symptoms of ascites or pericardial and pleural serous effusions which can persist for years in undiagnosed cases and respond rapidly to thyroxine when serum-T.S.H. returns to normal. Lack of thyroxine is not the cause of these features since they are not found in pituitary myxoedema, where thyroid hormone levels are as low but T.S.H. is absent.
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PMID:Possible stimulation of thermogenesis in brown adipose tissue by thyroid-stimulating hormone. 4 49

Thyroid hormone formation requires the coincident presence of peroxidase, H2O2, iodide, and acceptor protein at one anatomic locus in the cell. The peroxidase enzyme appears to be a protoporphyrin lX containing heme protein, with binding sites for both iodide and tyrosine. It is probable that both iodide and tyrosine are oxidized to free radical forms which unite to form iodotyrosine. The peroxidase is also involved through an uncertain mechanism in iodotyrosine coupling and probably in oxidation of sulfhydryl bonds in thyroglobulin. H2O2 may be supplied by microsomal NADPH-cytochrome c reductase or NADH-cytochrome b5 reductase. Other possible intracellular H2OI generating systems include monoamine oxidase and xanthine oxidase. The usual acceptor for iodide is thyroglobulin, which is currently believed to be iodinated within apical secretory vesicles at the cell border just prior to liberation into the colloid, or possibly after liberation into the colloid. Other soluble an insoluble proteins are also iodinated within the gland. The peroxidase is present in numerous cellular structures, but iodination activity occurs primarily, if not only, at the apical cell border. The controls of iodination are imperfectly known. Thyrotrophin modulation of iodide uptake, H2O2 generation, thyroglobulin synthesis, and peroxidase enzyme level obviously are the main regulations. Many of these actions are thought to involve mediation of adenyl cyclase and subsequent activation of intracellular phosphokinases. Antithyroid drugs of the thiocarbamide group are competitive inhibitors of iodination under some circumstances, but if much iodide is present, they react with the oxidized iodine intermediate and are irreversibly inactivated themselves. Clinical problems involving defective peroxidase function are among the most frequent hereditary defects of thyroid hormone formation. Recognized abnormalities include deficient peroxidase, abnormality in binding of the peroxidase apoprotein to its prosthetic group, and other less well-identified abnormalities in peroxidase structure and function. Peroxidase is typically elevated in thyroid tissue from patients with hyperthyroidism sometimes deficient in cold thyroid nodules, and frequently diminished in tissue from patients with Hashimoto's thyroiditis.
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PMID:Biosynthesis of thyroid hormone: basic and clinical aspects. 6 47

A patient with a toxic adenoma, already reduced in size by TSH, presented on the third day after treatment of a common cold by phenylpropanolomine, a severe pain in the thyroid gland. 4 weeks later, the nodule, which measured 3 x 4 cm. had clinically disappeared and the scan returned to normal. The disappearance 5 months later of the antithyroid antibodies confirmed the cure. Catecholamines, stimulating the production of thyroid hormone and producing temporary ischemia of the gland, phenylpropanolamine, a sympathomimetic drug, may have caused hemorrhagic necrosis of the adenoma and its disappearance.
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PMID:[Evanescent toxic thyroid adenoma. Possible role of phenylpropanolamine]. 20 Oct 31

The importance of the monodeiodination of T4 to T3 in the physiological action of T4 was explored by assessing the role of T4 in maintaining prophylthiouracil (PTU)-treated rats during exposure to 4 degrees C. (PTU inhibits both thyroid hormone biosynthesis and T4 to T3 conversion in peripheral tissues.) Firstly, the effects of cold exposure on the metabolism of T4 in control and PTU-treated rats equilibrated with [125I]T4 (2 microgram/100 g b. w./day) were determined. PTU was administered in the food (2 mg/g food). In control rats, no significant changes in T4 metabolism occurred during 3 days at 4 degrees C. Urinary 125I was greatly decreased in PTU-treated rats. Exposure of these rats to cold resulted in some increase but values were still 50% below normal. Secondly, four groups of rats were exposed to cold: control; PTU-treated; T4-treated; PTU + T4-treated. Control and T4-treated rats survived. PTU-treated rats died unless T4 was administered. Radioimmunoassay of T4 and T3 indicated significant concentrations of T3 in sera of rats from all but the PTU + T4 group. These results suggest that T4 permits survival in the cold-exposed PTU-treated rat without being converted to T3 and thus they support the concept that T4 has intrinsic biological activity.
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PMID:Thyroxine: studies concerning its intrinsic physiological activity. 58 May 39

Every patient with myxedema has hypothyroidism, but not every hypothyroid patient has myxedema. It often is possible to diagnose myxedema on clinical grounds alone. Characteristic symptoms are weakness, cold intolerance, mental and physical slowness, dry skin, typical facies, and hoarse voice. Results of the total serum thyroxine and free thyroxine index tests usually will confirm the diagnosis. L-thyroxine is the treatment of choice for myxedema, but it must be given to elderly patients with extreme caution. The transition from the hypothyroid to the euthyroid state brings about changes that put an added burden on the heart. The patient's clinical status and results of thyroid function tests determine the proper maintenance dose. Myxedema coma is rare but often fatal. It occurs most often in elderly women and may be mistaken for one of the chronic debilitating diseases common to this age group. Primary treatment is prompt administration of adequate doses of thyroid hormone--either l-throxine given intravenously of L-triiodothyronine given by nasogastric tube. It also is essential to identify and treat the condition precipitating the coma.
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PMID:Diagnosing and treating myxedema and myxedema coma. 62 51

Analysis by x-ray fluorescence allows in vitro determination of iodine content of the thyroid gland and a mapping of the regional distribution of iodine in the gland. The picture produced is similar to that of the conventional radioisotope thyroid scan. In 5 normal subjects and 70 patients with thyroid disease, the thyroid concentration of iodine varied between undetectable and 28 mg. With the exception of hypothyroid patients, who showed low thyroid levels of iodine, all patients showed iodine values overlapping the normal range. The fluorescent scan gave results similar to those of the isotope scan in most cases. Exceptions were noted in some hypothyroid patients, patients with flooded iodine pool, and patients receiving suppressive doses of exogenous thyroid hormone. Small cold nodules were best detected by the radionuclide scintigram. The value of the fluorescent scan is in its low radiation dose and in the possibility it affords of studying patients whose thyroid glands have reduced uptake of the radioactive tracer.
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PMID:Fluorescent thyroid scanning. A method based on stable iodine measurements. 62 25

The highly sensitive thermometric method (1.10(-5) degrees C/mm) revealed that the heat production of single contraction of the isolated rat diaphragmal muscle with artificial hyperthyrosis (HD) is nearly double of that of the normal muscle (ND). Noradrenaline added to the inculation solution entailed a greater increase of heat production of the muscle contraction in HD and had no significant effect on ND. However, calorific effect of thyroid hormone was about twice and a half as great as that of noradrenaline. These data suggest that thyroxin acts independently in the energy regulation during the cold acclimation of the organism, and the calorific effects of both hormones can be more effectively realized just at the moment of muscle contraction.
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PMID:[Effect of thyroxine and noradrenaline on the energetics of muscle contraction]. 68 3

To investigate the physiology of thyrotropin-releasing hormone (TRH) secretion from hypothalamus and brain, a method for measurement of peripheral plasma TRH concentrations in rats was developed. Blood was collected in heparin and dimercaptopropanol containing [3H]TRH to determine recovery. The plasma was extracted with methanol and the redissolved dried methanol extracts applied to anti-TRH Sepharose columns. These columns bound greater than 80% of 125I-TRH applied and had a capacity in excess of 20 ng TRH. TRH was eluted from the anti-TRH Sepharose with acetic acid and quantitated by radioimmunoassay of the lyophilized acetic acid eluate. Mean recovery of unlabeled TRH was 44.7+/-6.1% (SD) and mean recovery of [3H]TRH was 44.0+/-4.0%. Mean plasma TRH concentrations, corrected for recovery, in plasma pools from eight groups of normal male rats (four to seven pools/experiment, five to seven rats/pool) ranged from 7 to 30 pg/ml (mean, 16). In experiments in which rats were given 5, 10, 15, 0r 50 mug thyroxine daily for 1 wk or in thyroidectomized rats, mean plasma TRH concentrations did not differ significantly from those of control animals sacrificed at the same time. In each experiment, four to seven plasma pools, each from five to seven rats, were processed from both control and experimental groups. No changes in plasma TRH concentrations were found in rats exposed to cold (4degreeC) for 30, 60, and 90-180 min. Signigicant increases in plasma thyrotropin (TSH) concentrations were found in all cold-exposed animals. These results provide no evidence that thyroid hormone excess of deficiency affects TRH secretion. If TRH secretion is responsible for cold-induced increases in plasma TSH concentrations, the increase in TRH secretion is of insufficient magnitude to alter periperal plasma TRH concentrations.
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PMID:Plasma thyrotropin-releasing hormone concentrations in the rat. Effect of thyroid excess and deficiency and cold exposure. 81 90

The evolutionary transition from poikilothermy to homeothermy required the recruitment of complex mechanisms that provided both higher rates of heat production and regulation of heat loss in the presence of wide variations in ambient temperature. Two pathways that have been considered to be contributors to the transition to homeothermy are thyroid-regulated thermogenesis and nonshivering thermogenesis in the adaptation to cold. These pathways may yield higher rates of heat production in homeotherms by two processes that need not be mutually exclusive: a) hydrolysis of ATP and consequent generation of the Pi acceptor--ADP, or b) decreased coupling of mitochondrial oxidative phosphorylation. A significant fraction of both thyroid and catecholamine thermogenesis has been ascribed to enhanced energy expenditure in active transmembrane Na+ transport (i.e., the Na+ pump). By extension these findings implicate the Na+ pump as a heat source in the evolution of the homeotherms. The thermogenic response to thyroid hormone is both rapid and profound in homeotherms (mammals), and more slowly evident and probably lesser in magnitude in poikilotherms (amphibia and reptiles). One crucial pathway in the evolution to homeothermy may be nonshivering thermogenesis in response to cold. In mice, most of the elevated rate of oxygen consumption of liver and skeletal muscle elicited by cold exposure is ouabain-sensitive. Thus, the Na+ pump appears to be an important heat source in the transition to homeothermy. The underlying biochemical mechanisms that mediate the contribution of the Na+ pump to heat production, including responsiveness to thyroid hormone and catecholamines, however, may not be unique to the homeotherms.
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PMID:Transition from the polikilotherm to the homeotherm: possible role of sodium transport and thyroid hormone. 94 96

Rats raised from day 2 of life at an ambient temperature of 10 degrees showed delayed vaginal opening when compared to controls raised at 22 degrees. Cold-raised animals were also lighter in weight at the time of vaginal opening and had significantly longer estrous cycles. Low temperature may cause these effects either by suppressing prolactin secretion or, more probably, by elevating thyroid hormone levels which in turn suppress serum gonadotropin concentrations.
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PMID:Vaginal opening and early estrous cycles in rats raised at a low ambient temperature. 98 11


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