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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 a sudden but sustained exposure to cold (1 to 6C) on serum TSH, thyroxine (T4) and triiodothyronine (T3) (all measured by radioimmunoassay), pituitary TSH concentration, pituitary TSH secretory responsiveness to hypothalamic extract or synthetic thyrotropin-releasing hormone (TRH) in vitro as well as in vivo, and the changes of the thyrotropin-releasing activity in three TRF-rich hypothalamic areas were determined. In normal animals, serum TSH underwent a series of oscillations, first rising then returning to the basal levels, then rising again, whereas serum T4 and T3 increased within 2 h of cold exposure and remained elevated. Pituitary TSH concentration and the in vitro pituitary responsiveness declined after an initial elevation, whereas the in vivo responsiveness to TRH was diminished throughout the whole exposure to cold. Thyroid-blocked animals with steady, low levels of serum T4 and T3 showed a step by step increase of serum TSH levels and no changes in the other parameters. It is therefore assumed that the decrease of TSH secretion following the initial rise is due to a feedback inhibition by the increased levels of thyroid hormones as is the decreased pituitary responsiveness of TRH in vivo. The pituitary responsiveness in vitro seems to be determined by TSH pituitary concentrations, the changes of which are probably also secondary to the changes of the thyroid hormone levels. The mechanism of the second rise of serum TSH levels is not clear. Thyrotropin-releasing factor (TRF) activity was higher after 2 and 24 h of cold exposure in the median eminence and after 8 h in the anterior hypothalamus-preoptic area, but lower after 8 and 24 h in the dorsomedial hypothalamus. Since the changes of TRF activity in the median eminence coincided with the elevated serum TSH, they are assumed to reflect increased TRF production and secretion. The significance of the TRF changes in the other two areas is not clear.
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PMID:Effect of acute exposure to cold on the activity of the hypothalamic-pituitary-thyroid system. 118 7

Forty-five male, weanling Sprague-Dawley rats were matched by weight into three groups (n = 15). One group was fed ad libitum a semipurified diet containing all essential nutrients and 30 ppm of zinc (control). A second group was fed ad libitum a similar diet but with a deficient zinc intake of less than 1 ppm (ZnD). A third group was pair-fed (PF) the control diet in amounts equal to that consumed by the matched ZnD animals. After 42 days, the animals were fasted for 12 hr then five animals from each group were sacrificed and the remainder was exposed to 3 degrees C for 6 hr. Rectal temperatures were lower (p less than 0.05) in ZnD at 23 degrees C and during cold exposure. Plasma thyroxine (T4) and triiodothyronine (T3) concentrations were reduced (p less than 0.05) at room temperature in ZnD rats. During cold exposure, the ZnD animals had depressed (p less than 0.05) plasma thyrotropin, T4 and T3 concentrations. Thus, ZnD adversely affects thermoregulatory performance of rats acutely exposed to cold by influencing thyroid hormone metabolism.
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PMID:Impaired thyroid hormone status and thermoregulation during cold exposure of zinc-deficient rats. 152 22

Whole blood hematocrit (HCT) decreases during multiple exposures to cold air. To better understand this finding, we have analyzed hematological profiles in 27 normal adult men exposed repeatedly to cold air in one of two experimental protocols. Experiment I was a cold air acclimatization study (CAA) conducted with two groups of 8 men in each group before, during, and after 80 separate 30-minute cold (4 degrees C) air exposures. As part of a metabolic study, half of the men received placebo daily (n = 8), and the other half received an oral daily maintenance dose of the thyroid hormone triiodothyronine (T3) (30 micrograms/day). Blood was analyzed prior to and after every 20 cold exposures. Both groups reacted similarly. When compared with basal conditions, hematocrit (HCT) and erythrocyte counts (RBC) were decreased (p less than 0.05); mean corpuscular hemoglobin concentration (MCHC) and plasma volume (PV) were increased with cold exposure (p less than 0.05). Hemoglobin (Hb), leukocyte counts (WBC), and mean corpuscular volume (MCV) were unchanged. Experiment II was carried out with 9 military volunteers during extended arctic winter field operations (EAO) in Utah and Alaska. Blood was analyzed prior to and after completion of EAO. A changing hematological profile similar to that in the CAA protocol was found. Hematocrit and RBC were decreased (p less than 0.02); MCHC and PV were increased (p less than 0.02). Hemoglobin, WBC, and MCV were unchanged. In addition, there was a negative correlation between HCT and the absolute reticulocyte count in this second experiment. It would appear that in instances of cold stress, whether induced or naturally occurring, certain blood cellular elements respond in a similar adaptive manner.
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PMID:Hematological parameters are altered during cold air exposure. 156 90

A tumor appeared on the back of a transgenic mouse carrying the SV40 T-antigen under control of a mouse major urinary protein promoter. High levels of mRNA for the mitochondrial uncoupling protein (UCP) indicated that the tumor was a hibernoma. The tumor has been established as a transplantable tumor line in nude (nu/nu) mice and used as a source of cells to develop a tissue culture system for analyzing brown fat development and differentiation. Ucp expression in tumor cells cultured in Dulbecco's modified Eagle's medium and 10% fetal calf serum was virtually undetectable. Addition of 10(-7) M norepinephrine resulted in approximately a 30-fold induction of Ucp mRNA within 4 h. The induction by norepinephrine was independent of cell density and also independent of thyroid hormone and insulin during the first 5 days in culture. However, in order to maintain the inducibility of Ucp during prolonged culture periods, it was necessary to supplement the medium with insulin. In contrast to Ucp, the expression of Gdc-1, which encodes the cytoplasmic glycerol-3-phosphate dehydrogenase and which is also induced in brown fat by cold exposure, was repressed by norepinephrine and induced by the addition of insulin. Characterization of the adrenergic receptors required for Ucp induction with agonists and antagonists indicated that beta 1 receptors are predominantly utilized; there is no evidence for utilization of beta 3 and alpha 1 receptors for Ucp induction.
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PMID:Adrenergic regulation of the mitochondrial uncoupling protein gene in brown fat tumor cells. 160 85

This study examined the effect of prolonged physical activity in a cold environment upon circulating thyroid hormone levels. A secondary focus of the study involved the role of nocturnal habitat upon the thyroidal responses to the physical activity and cold exposure. Military personnel exposed to 10 d of field-based operations in the arctic region of Norway were studied. Blood samples were collected before (day 1), and at days 5 and 10 of the operations. Levels of total T4, free T4, total T3, free T3, and thyroid binding globulin were assessed in all blood samples. The results indicated considerable, significant (p less than 0.05) decreases in total thyroid hormone levels, while relative increases of free fractions of the hormones occur with the 10-d operations in the Arctic. However, no significant influence on thyroidal responses were observed due to the nocturnal habitat that the subjects lived in. The hormonal alterations noted are possibly brought about by the combined effects of physical activity and cold exposure acting synergistically to alter thyroid physiology (e.g., most likely the protein carrier binding affinity).
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PMID:Thyroid hormone changes during military field operations: effects of cold exposure in the Arctic. 161 37

The effects of cold exposure on the release of thyrotropin-releasing hormone (TRH) and catecholamines as estimated by push-pull perfusion of the mediobasal hypothalamus were studied. Before cold exposure, the male rats had been kept at room temperature or at 30 degrees C for 3 weeks. Transfer to 4 degrees C increased plasma levels of thyroid-stimulating hormone (TSH), but this cold-induced TSH response was more pronounced in animals which had been acclimatized to 30 degrees C. Exposure to 4 degrees C also increased plasma thyroid hormone levels, but had no effect on plasma prolactin. The hypothalamic content of TRH and dopamine remained similar after transfer to 4 degrees C, but after 6 h of cold, the content of noradrenaline and adrenaline had increased 1.6-fold and 3-fold, respectively. In vivo hypothalamic release of TRH, adrenaline and dopamine remained similar during a 2-hour period in control rats kept at room temperature or 30 degrees C. The hypothalamic release of TRH, dopamine and adrenaline did not change in rats transferred from room temperature to 4 degrees C. The amount of dopamine and adrenaline in push-pull perfusate also remained similar in rats acclimatized to 30 degrees C after transfer to low temperatures. However, in these rats kept at 30 degrees C for 3 weeks, exposure to 4 degrees C increased TRH release in perfusate from the mediobasal hypothalamus in the first 15 min of cold exposure (2-fold increase). Thus, exposure to cold stimulates the hypothalamo-pituitary-thyroid axis and increases the hypothalamic release of TRH in rats which had been acclimatized to 30 degrees C.
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PMID:Effect of cold exposure on the hypothalamic release of thyrotropin-releasing hormone and catecholamines. 174 62

In animals, decreases in selenium-containing glutathione peroxidase activity and the resultant impairment of peroxide metabolism can account for many, but not all of the biochemical and clinical changes caused by selenium deficiency. Recently, however, type I iodothyronine 5'-deiodinase has also been shown to be a selenium-containing enzyme. This explains the impairment of thyroid hormone metabolism caused by selenium deficiency in animals with a normal vitamin E status. Since iodothyronine 5'-deiodinases are essential for the production of the active thyroid hormone 3,5,3'-triiodothyronine, some of the consequences of selenium deficiency may result from thyroid changes rather than inability to metabolise peroxides. In particular, the impaired thyroid hormone metabolism may be responsible for decreased growth and resistance to cold stress in selenium-deficient animals. A further consequence of the role of selenium in thyroid hormone metabolism is the exacerbation of some of the thyroid changes in iodine deficiency by a concurrent selenium deficiency. Selenium status may therefore have a major influence on the outcome of iodine deficiency in both human and animal populations.
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PMID:The role of selenium in thyroid hormone metabolism. 180 11

A depressive man was evaluated for developing chronic fatigue and cold intolerance, in whom laboratory findings showed decreased thyroid hormone levels (T4, 2.7 micrograms dl-1; T3, 0.76 ng ml-1) with normal blood levels of TSH. A single bolus injection of TRH (500 micrograms) significantly stimulated prolactin secretion, but did not cause an increase in blood TSH levels (basal level, 1.2 microU ml-1 vs. 1.3 microU ml-1 30 min after injection). By contrast, TRH-induced TSH stimulation occurred after repeated injection of TRH for 4 consecutive days (basal level, 1.5 microU ml-1 vs. 5.6 microU ml-1 30 min after injection). Blood thyroid hormone concentrations were restored to normal levels after long-term administration of TRH. Other pituitary functions remained unchanged. A diagnosis of central hypothyroidism due to isolated TRH deficiency was made in this case, and the data presented here indicate that partial resistance of pituitary thyrotrophs to TRH may be associated with depression.
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PMID:Central hypothyroidism due to isolated TRH deficiency in a depressive man. 190 Oct 77

A microscale method, based on two-colour dye immunolabelling and flow sorting cytofluorometry, was used to characterize lymphocyte subsets in thyroid tissue specimens obtained by fine-needle aspiration (FNA) in 21 patients with autonomously functioning thyroid nodule (AFTN) and five patients with cold thyroid nodule (CTN). Inversion of the ratio between CD4+ and CD8+ lymphocytes, due to a relative increase of CD8+ cells, was found among intrathyroidal lymphocytes in AFTN patients. The abnormal lymphocyte subset distribution was not observed in the peripheral blood of the same group of patients. In patients with CTN the lymphocyte subset distribution was normal, both in the thyroid and in the peripheral blood. In AFTN patients, a significant correlation was observed between the decrease of intrathyroidal CD4+/CD8+ ratio and the increase of plasma thyroid hormone levels. Whether the immunological abnormalities found in AFTN could play a pathogenetic role in the clinical presentation and outcome of the disease remains to be established. The FNA-applied micromethod used in this study could be extended as a routine investigation to characterize the immunogenic substrate of thyroid disorders.
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PMID:Cytofluorometric analysis of lymphocyte subsets in thyroid aspirates from patients with autonomously functioning nodules. 197 83

As judged by the response of uncoupling protein and key enzymes, brown adipose tissue (BAT) is highly dependent upon the local generation of T3 catalyzed by the tissue type II T4 5'-deiodinase (5'-D-II). In hypothyroid rats treated with T3 or T4, the capacity to withstand cold seems better correlated with the normalization of BAT responses than with the liver thyroid status. 5'D-II is activated by cold via sympathetic nervous system (SNS) stimulation, and the activation generates enough T3 to nearly saturate BAT nuclear T3 receptor (NTR) in euthyroid rats. In hypothyroidism, 5'D-II is highly stimulated by the SNS and hypothyroxinemia. In the present studies we have taken advantage of this situation to test 1) the capacity of 5'D-II to maintain nuclear T3 in rats with various degrees of hypothyroxinemia, and 2) the hypothesis that thyroid hormone-dependent BAT-facultative thermogenesis, rather than the effect of thyroid hormone on obligatory thermogenesis (basal metabolic rate), is the basic mechanism by which thyroid hormone confers protection against acute cold exposure. We treated methimazole-blocked rats (undetectable plasma T4 and T3) for a week with either subreplacement doses of T4 (0.5, 1, 2, and 4 micrograms/kg.day) or replacement doses of T4 or T3 (8 or 3 micrograms/kg.day, respectively). Sources and content of BAT nuclear T3 were studied at 25 C and after 48 h at 4 C by labeling the plasmaborne T3 (T3[T3]) with [131I]T3 and the locally generated T3 (T3[T4]) with [125I]T4. Neither the kinetics of nuclear-plasma exchange of T3[T3], the time of appearance of T3[T4] in BAT nuclei, nor NTR maximal binding capacity (0.71 ng T3/mg DNA) was affected by hypothyroidism. Kinetic analyses indicated a maximal BAT NTR occupancy of 40% at euthyroid serum T3 concentrations if T4 is not present. Replacement with T4 normalized both serum T4 and T3, while replacement with T3 normalized serum T3; for all other doses of T4, serum T4 and T3 concentrations were predictably related to the dose. 5'D-II activity decreased with increasing doses of T4, but for each dose of T4, this activity was 2-4 times greater at 4 C than at 25 C. BAT NTR occupancy normalized with 2 micrograms T4/kg in rats maintained at 25 C and with 4 micrograms T4/kg in cold-exposed rats, although in neither condition were serum T4 and T3 normalized nor more than 30% of NTR occupied by plasma T3.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central role of brown adipose tissue thyroxine 5'-deiodinase on thyroid hormone-dependent thermogenic response to cold. 200 19


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