UMLS:C0009443 - FACTA Search

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Query: UMLS:C0009443 (cold)
92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of alpha-neoendorphin, kyotorphin, melatonin or diphenylhydantoin (DPH) on thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) release in rats were studied. alpha-neoendorphin (1.0 mg/kg), kyotorphin (1.0 mg/kg), melatonin (2.5 mg/kg) or DPH (75 mg/kg) was injected iv or ip, and the rats were serially decapitated. TRH, TSH and thyroid hormone were determined by radioimmunoassay. The hypothalamic immunoreactive (ir-TRH) contents decreased significantly after melatonin injection, but not after alpha-neoendorphin, kyotorphin or DPH. The plasma ir-TRH concentrations decreased significantly after DPH injection, but not after alpha-neoendorphin, kyotorphin or melatonin. The plasma TSH levels decreased significantly in a dose-related manner with a nadir at 10 min. after melatonin, at 30 min. after DPH and at 40 min. after alpha-neoendorphin or kyotorphin injection. The plasma thyroid hormone levels did not change significantly after these drugs injection. The plasma ir-TRH and TSH responses to cold were inhibited by these drugs, but the plasma TSH response to TRH was not influenced. In the L-DOPA- or 5-hydroxy-tryptophan (5-HTP)-pretreated group, the inhibitory effect of alpha-neoendorphin or kyotorphin on TSH levels was prevented, but not in the haloperidol- or para-chloprophenylalanine (PCPA)- pretreated group. In the haloperidol- or PCPA-pretreated group, the inhibitory effect of melatonin on TSH levels was prevented, but not in the L-DOPA- or 5-HTP-pretreated group. These drugs alone did not affect plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity by hypothalamus or plasma in vitro after these drugs injection did not differ from that of the control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of various drugs on thyrotropin secretion in rats. 316 12

Mild cold exposure (22 degrees C, with reference to 28 degrees C, thermoneutral) was studied by overnight whole-body indirect calorimetry in euthyroid women. Basal, sleeping, energy expenditure (EE) was significantly increased (+3.8%, P less than 0.05) in six normal weight women but reduced (-3.5%, P less than 0.05) in five obese type II diabetic women. Mixed responses were found in five women with simple obesity. Biochemical measurements were made on fasting blood samples taken at 0900 h after 12 h exposure to the two temperatures. Serum T4, free T3 and TSH were within the normal reference range in all subjects. Serum T4 did not show any differences between the groups, nor any effect from temperature. There was a significant increase in free T3 (P less than 0.05) at 22 degrees C in the control subjects, but no differences in the obese diabetic women. Serum thyroglobulin fell significantly in the diabetic group. Both TSH and free T3 responses to mild cold were significantly different between the groups, but both correlated positively (P less than 0.05) with the changes in sleeping energy expenditure at 22 degrees C with reference to 28 degrees C. Changes in TSH and free T3 were themselves significantly correlated within individuals (P less than 0.01). The normal physiological non-shivering thermogenesis of adult humans on exposure to a cool environment may thus be mediated by a pituitary-thyroid mechanism. The abnormal response of obese diabetic women was associated with impaired TSH and thyroid hormone responses, and may be a factor contributing to weight gain.
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PMID:Metabolic and thyroidal responses to mild cold are abnormal in obese diabetic women. 325 62

Danowski et al. (1951) were probably the first who showed an increase of PBI in infants shortly after birth. Later a number of investigators presented further evidence on the increased thyroid gland function in newborns. This condition named "neonatal thyroid hyperactivity" [Fisher and Oddie, 1964] was described also in animals. The available data indicate that all the newborn mammals till now studied, independently of the maturation stage of development they reach at birth, display some features of thyroid hyperactivity, but in some it does not lead to hyperiodothyroninaemia. Interspecies differences coincide well with significance of the thyroid hormones for neonatal thermogenesis. There are few sequential studies of the three principal iodothyronines: T4, T3 and rT3 available at present. The most comprehensive data concern infants, newborn lambs and pigs. Immediately after birth, there is a sudden rise in serum thyroid hormone concentrations, with some species differences related to the degree of the increase and to the iodothyronines involved. The course of the postnatal hyperiodothyroninaemia is dependent on the maturation level reached at birth, food intake, and cooling relative to extrauterine environment. At least five main factors contribute to the immediate postnatal hyperiodothyroninaemia: 1) abrupt depletion of the preformed fetal hormonal iodine stores; 2) preferential T3 secretion; 3) increase in the T4 to T3 monodeiodination in the peripheral tissues; 4) a release of thyroid hormone content from peripheral reservoirs to plasma, and 5) action of other hormone(s) concomitantly released at birth. From the point of view of the thermal adaptability, the newborn mammals fall into two distinct groups: first, in which immediately after birth the metabolic rate decreases, and second, in which the metabolic rate increases, after cooling. Our understanding of the role and significance of hormonal factors involved in mechanisms of the postnatal thermogenesis is incomplete. However, some similarities in adaptation to cold in adults and in newborns seem to be relevant. Cold adaptation is accomplished by development of nonshivering thermogenesis (NST) depending on NA. The presence of brown adipose tissue (BAT) is essential for NA thermogenic action. According to the common opinion, based on data from laboratory animals and human baby, non-shivering thermogenesis, but not shivering, predominates in newborns. However, data from domestic animals indicate that shivering thermogenesis may be of comparable or greater thermogenic capacity than NST at birth. Besides, there are some newborns which have little or no BAT and associated NST.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hyperiodothyroninaemia of neonates, its significance for thermogenesis. 325 52

In the chicken the transition of a poikilotherm to a homeotherm reaction upon cold exposure takes place in the perinatal period between pipping and hatching. However, newly hatched chicks cannot maintain their body temperature within narrow limits after cold exposure. The fact that relatively little attention was payed on the role of thyroid hormones in the thermoregulatory reaction to cold of young chicks was probably due to the hypothetically long latention time that was thought to be necessary to bring about changes in secretory activity by cold stimulation. However, more recently, rapid changes (within hours) of thyroid hormone concentrations upon cold exposure were described in the chickens and the quail. In this study, changes in circulating T3 and T4 concentrations upon cold exposure of young chicks during the first two weeks were followed, that means during the period wherein NST (non-shivering thermogenesis), if it exists at all, should be progressively replaced by ST (shivering thermogenesis). Because of the importance of feeding condition on thyroid hormone levels, the experiments were carried out with and without a preceeding fasting period. In all experiments a short-term cold exposure of young chickens (1-11 days) fed ad lib decreased T3 but increased T4 levels while a reversed picture was found after short cold exposure of the fasted animals. However, after prolonged cold stimulus (15 degrees C) of young chickens fed ad lib, plasma T3 was also significantly elevated over that of controls whereas T4 levels returned to normal values. A prolonged warm treatment (37 degrees C) of young chickens fed ad lib resulted in significantly lower T3 and higher T4 concentrations. After a prolonged cold treatment no differences in T4 or T3 response upon TRH were found whereas the warm treatment abolished these responses upon TRH. However, a cold treatment at the stage of incubation during which the hypothalamo-hypophyseal control of thyroid function is established (dag 10-14) enhanced the T4 response to TRH with a long lasting effect extending to the posthatch period. Since T3 is thought to be the active form of thyroid hormones with regard to thermopoiesis we have studied more specifically the effect of blocking peripheral conversion of T4 on thermoregulatory abilities in young chicks and the influence of temperature treatment on monodeiodination capacity. The lower rectal temperatures following the interference with the peripheral monodeiodination of T4, the effect being more pronounced at the lower ambient temperature, are indicative for a preponderant role of T3 on thermogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in thyroid hormone physiology induced by temperature and feeding in newly hatched chickens. 325 53

It is clear that thyroid hormones modulate non-shivering heat production of the newborn mammal. While some obvious thyroid hormone effects on thermogenesis can be demonstrated in adult, cold-acclimated or hibernating animals, these findings cannot be directly applied to the newborn, in which changes in amount and composition of brown adipose tissue, as well as sympathetic and thyroid system maturational events, are occurring. Thyroid hormones do influence the prenatal development and subsequent responses of brown adipose tissue in neonates through primary actions on brown adipose tissue iodothyronine 5'monodeiodinase and mitochondrial uncoupling protein. Secondary effects involving brown adipocyte growth, lipid composition, oxidation proteins, and sympathoadrenal activity are of lesser importance in thyroid hormone modulation of newborn thermogenesis. The acute surge in thyroid hormones that occurs at birth seems of limited significance with regard to neonatal thermogenesis. The stimulation of sympathoadrenal activity at the time of birth, as well as continued in situ conversion of T4 to T3 in the brown adipocyte, are of critical importance in stimulating and modulating heat production in the newborn.
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PMID:Thyroid hormone effects on neonatal thermogenesis. 329 26

Hepatic nuclear triiodo-L-thyronine (T3) receptors were studied to investigate the mechanism of thyroid hormone resistance in Richardson's ground squirrels, Spermophilus richardsoni, during the hibernation phase of the annual cycle. The cycle is divided into an active phase and a hibernation phase, the latter composed of alternating dormancy and arousal bouts. In addition to animals in these three states, a group of cold-exposed animals was also examined (those animals held at 6 degrees which showed no indications of entering hibernation). Binding of T3, to squirrel hepatic nuclei from all groups, was characterized as high affinity, Kd ranging from 111 to 267 pM, and low capacity, 50 to 314 fmol T3/mg DNA. Based on these data, other criteria examined, and models established in the literature for other species, this binding site has been tentatively identified as a T3 receptor. Receptor concentrations in nuclei from dormant and aroused squirrels were only 15-20% of the concentration in active animals. There were no differences in the affinity of the T3 receptor over the annual cycle estimated by the in vitro assay at 24-26 degrees. The reduction in nuclear T3 receptors, together with the previously reported increase in serum binding of thyroid hormone, provides an explanation for thyroid hormone resistance during the hibernation phase in S. richardsoni.
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PMID:Thyroid hormone resistance in hibernating ground squirrels, Spermophilus richardsoni. II. Reduction of hepatic nuclear receptors. 336 Feb 94

In liver, thyroid hormone rapidly induces S14 mRNA, which encodes a small acidic protein. This sequence is abundantly expressed only in lipogenic tissues and is thought to have some function in fat metabolism. In the euthyroid rat, we measured 20-fold higher levels of S14 mRNA in interscapular brown adipose tissue than liver. Furthermore, whereas in liver or epididymal fat, hypothyroidism resulted in an 80% fall in S14 mRNA, in brown fat the level of this sequence increased a further 3-fold. In all three tissues, the expression of S14 mRNA correlated well with lipogenesis, as assessed by 3H2O incorporation. Physiological activation of brown fat by chronic cold exposure or cafeteria feeding increased the concentration of S14 mRNA in this tissue and again this was accompanied by a greater rate of fatty acid synthesis. Overall, in liver and white and brown adipose tissue, S14 mRNA and lipogenesis were well correlated and strongly suggest a function of the S14 protein related to fat synthesis. These studies suggest that the S14 protein and lipogenesis may be important for thyroid hormone-induced and brown adipose tissue thermogenesis and that stimulation of these functions in hypothyroid brown fat is a consequence of decreased thyroid hormone-induced thermogenesis elsewhere.
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PMID:Stimulation of S14 mRNA and lipogenesis in brown fat by hypothyroidism, cold exposure, and cafeteria feeding: evidence supporting a general role for S14 in lipogenesis and lipogenesis in the maintenance of thermogenesis. 347 52

The effects of prostaglandin A1 and A2 (PG A1, A2) on secretion of thyrotropin (TSH) in vivo and in vitro were studied. Hundred micrograms per kg of PG A1 and A2 were injected i. v., and the animals were serially decapitated. Thyrotropin-releasing hormone (TRH), TSH and thyroid hormone were determined by radioimmunoassay. Effects of Pg A1 and A2 from anterior pituitary gland were also investigated by means of an in vitro experiment. Plasma and hypothalamic concentrations of immunoreactive TRH (ir-TRH) did not change after PG A1 and A2 injection. Basal plasma TSH levels significantly increased with a peak at 20 min after PG A1 and A2 injection. The plasma ir-TRH response to cold did not differ from that of the control, while the plasma TSH response to cold was significantly enhanced by PG A1 and A2. The plasma TSH response to TRH was also enhanced by PG A1 and A2. The plasma thyroid hormone did not change significantly after PG A1 and A2 injection. TSH release from anterior pituitary in vitro significantly increased after the addition of PG A1 and A2 to medium. These findings suggest that PG A1 and A2 stimulate TSH secretion from anterior pituitary in vivo and in vitro.
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PMID:Effect of prostaglandin A1 and A2 on thyrotropin secretion in rats. 349 64

In order to study the effect of thyroid hormones on rat cerebellar granule cells, cerebellar perikarya isolated from 5-7-day-old rats were cultured in the presence of normal fetal calf serum, fetal calf serum treated with Dowex-2 ion exchange resin to remove thyroid hormones, or ion exchange-treated serum resupplemented with physiological concentrations of T4 and T3. Granule cells grown under hypothyroid conditions showed abnormal cellular aggregation, neurite fasciculation and cell survival. Cell aggregation, which may be an in vitro correlate of cerebellar granule cell migration to the internal granule layer, was reduced by over 50% under hypothyroid conditions. The rate of protein synthesis in hypothyroid cultures was stimulated by as much as 3-fold compared to thyroid hormone-containing cultures consistent with a proposal that the normal developmental pattern of diminishing protein synthesis specific activity is delayed or prevented under hypothyroid conditions. In addition ultrastructural studies revealed abnormalities in the density of cold-stable microtubules in thyroid hormone-deficient cultures. These results demonstrate that thyroid hormones can influence granule neuron behavior in the absence of Purkinje cells. Furthermore, the observed defects bear numerous similarities to documented abnormalities within the hypothyroid cerebellum, suggesting that this in vitro culture system may serve as a useful model for studying the mechanism of action of thyroid hormones on the cells of the cerebellum.
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PMID:Influence of thyroid hormones on rat cerebellar cell aggregation and survival in culture. 351 14

The effects of a diet including high-iodine eggs, containing much higher amounts of iodine than ordinary eggs, were investigated on lipid metabolism and thyroid function in rats. To a non-purified diet was added at the 1% (w/w) level ordinary egg power (OE diet: 35 micrograms iodine/100 g diet) or high-iodine egg powder (IE diet: 392 micrograms iodine/100 g diet). At 7 months and 19 months, feeding of the IE diet resulted in a lowered serum triacylglycerol level, elevated tissue lipoprotein lipase activity and a lowered lipid peroxide level in the brain. Although the serum total iodine level was 5 times higher in animals given the IE diet than in those given the OE diet, serum levels of thyroid-related hormones (TSH, T3 and T4) were not affected by feeding of the IE diet. In animals exposed to cold and given antithyroid drug treatment, the IE diet seemed to improve age-related defects in thermogenic and thyroid hormone responses to cold, and also to confer resistance to the antithyroid drug. These results suggest that iodine ingestion through high-iodine eggs modulates both lipid metabolism and thyroid function in rats.
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PMID:Nutritional implications of high-iodine egg diet in rats: effects on lipid metabolism and thyroid function. 359 39

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