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

The present studies examine the effect of starvation together with cold or hot exposure on thyroid hormone levels in rats. At 23 degrees C starved for 5 days, serum thyroid hormone levels decreased significantly compared with fed rats, averaging 3.6 +/- 0.5 micrograms/dl of thyroxine (T4), 47 +/- 11 ng/dl of triiodothyronine (T3), 1.4 +/- 0.3 ng/dl of free T4 and 39.6 +/- 5.1 pg/ml of reverse T3, respectively. At 15 degrees C rats starved for 5 days, serum free T4 level significantly more increased than that of 23 degrees C starved rats, while serum T4 level and T3 did not increase significantly. At 30 degrees C rats whether concomitant starvation or not, serum thyroid hormone levels of both group markedly more decreased than control rats. These experiment provide additional evidence that thyroid gland and the peripheral metabolism of thyroid hormone respond to variety situations such as cold or hot exposure together with starvation or not.
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PMID:[Factors affecting the serum thyroid hormone concentration during fasting in rats--with special reference to the relation with temperature]. 662 62

We studied the characteristics of monodeiodination of thyroxine to T3 and reverse T3 in the human placenta which was obtained at normal delivery. The placentas were homogenized in cold sucrose Tris-HCl buffer, pH 7.5. The microsomal fraction was incubated at 37 degrees C in the air for 1 hr with 2 micrograms of T4 in the presence of 0.05 M DTT. The T3 and reverse T3 generated in the reaction mixture were extracted into cold ethanol and measured by RIA. Among the usual subcellular fractions of the placental homogenate, microsomes were most potent in deiodinating T4 to reverse T3, 17.9 ng/mg protein/micrograms T4/60 min. In microsome, production of reverse T3 from T4 was dependent upon protein concentration, incubation temperature, incubation time, pH and T4 concentration, and unstable to prior heating of the microsomal fraction. The production of T3 from T4 was negligible in the present system. Degradation of T3 in the human placenta was rapid. Although addition of anti-T3 antibody to the reaction mixture suppressed the degradation of T3, it had no effect on the net production of T3, suggesting that the obtained net T3 production rate had not been influenced by its degradation. Degradation of reverse T3 was negligible. These results indicate that the human placenta actively deiodinates T4 to reverse T3 enzymatically. This enzyme system might have some influence on the transplacental passage of thyroid hormone from the mother to the fetus.
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PMID:Monodeiodination of thyroxine to 3,3',5'-triiodothyronine in the human placenta. 662 61

There are several mechanisms by which homeothermic animals increase heat production, including shivering, sympathetic nervous system activation and stimulation of thyroid hormone secretion. Studies in rats have shown that increased sympathetic activity causes increased heat production in brown adipose tissue (BAT) after cold exposure or food ingestion. Acute cold exposure also increases circulating thyroid hormones which in turn stimulate cellular metabolism through induction of various enzymes. Most metabolic effects of thyroxine (T4) are thought to be due to the triiodothyronine (T3) which is produced from T4 by a process of 5' monodeiodination. There are two enzymes responsible for this reaction: type I, or propylthiouracil (PTU)-sensitive iodothyronine deiodinase (5'D-I), which is reduced in hypothyroidism, stimulated in hyperthyroidism and probably provides most of the circulating T3 in the adult rat. Type II 5'-deiodinase (5'D-II) is characteristic of brain and pituitary, is increased by thyroidectomy, is not inhibited by PTU and provides 50-80% of the intracellular T3 in these two tissues. Recently, 5'D-II activity was identified in interscapular BAT. As the sympathetic nervous system influences the metabolic activation of BAT, we have studied the effects of noradrenaline and acute cold exposure on BAT 5'D-II. We report here that both noradrenaline and cold exposure increase BAT 5'D-II through alpha 1-adrenergic receptors, whereas depletion of catecholamines with alpha-methyl-p-tyrosine (MPT) prevents the effect of cold but not that of noradrenaline. These results suggest that the sympathetic nervous system may increase T3 production in rats by stimulating BAT 5'D-II. By increasing metabolic rate, this rise in T3 would enhance the thermogenic response to sympathetic stimulation.
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PMID:Adrenergic activation of triiodothyronine production in brown adipose tissue. 663 38

In 24 of 30 patients with lymphoma of the thyroid, the diagnosis was made preoperatively or without surgery; undifferentiated or poorly differentiated carcinoma was suspected in 3 other patients. Thirteen patients were under 60 years of age; 7 were under 40. An increase in the ratio of men to women was seen among younger patients. At presentation, a discrete nodule was found in 19 patients, and multinodular or diffuse goiters in 11. Seventy-six percent of patients with solitary nodules had enlargement of extranodular tissue. Imaging showed "cold" nodules, cold areas in diffuse goiters, or patchy uptake. Nine patients had obstructive complaints; 12 patients had subnormal thyroid function; 24 patients had coexistent Hashimoto's thyroiditis. Lymphoma of the thyroid was suggested by fine-needle biopsy results in 17 of 28 patients (undifferentiated carcinoma was suspected in 2); and by large-needle biopsy results in 21 of 23 (undifferentiated or poorly differentiated carcinoma was suspected in 2). Biopsy of diffuse Hashimoto's goiters is indicated for cold imaging defects, enlarging tender goiter, or goiter enlarging on thyroid hormone. Early diagnosis may improve prognosis for lymphoma of the thyroid, so that surgery or chemotherapy can be avoided.
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PMID:Lymphoma of the thyroid. 668 35

When exposed to an ambient temperature of 4 degrees C, iron-deficient anemic rats become hypothermic. This lesion is related more to anemia than to tissue iron deficiency, since exchange transfusion to hematocrits over 25 restored normal thermoregulatory performance. Likewise poor cold responses were induced in control rats by transfusion to low hematocrits. Cold sensitivity in all anemic animals was paralleled by poor thyroid responses: there was a significant positive correlation between hematocrit and percent rise in triiodothyronine (r = 0.63) and thyroxine (r = 0.53) during 6 h at 4 degrees C. Basal levels of thyroid-stimulating hormone (TSH) were similar in control and iron-deficient animals: after cold exposure, TSH rose to higher levels in those animals with hematocrits over 25 than in those with lower hematocrits. Diminished O2 delivery to tissues responsible for heat production is probably a major component of the cold sensitivity of anemic rats. The novel finding that thyroid hormone responses are compromised by anemia implies effects on hormonal regulation that may also contribute to this functional lesion.
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PMID:Effect of iron-deficiency anemia on hormone levels and thermoregulation during cold exposure. 674 20

The role of the pineal gland in the regulation of thyroid-stimulating hormone (TSH) secretion was studied in postpuberal male rats using 12:12 h light:dark cycles. Pinealectomy, performed 3--4 days before decapitation, had no effect on the basal or thyrotropin-releasing hormone stimulated TSH secretion, but significantly decreased the cold-induced TSH response both at noon and at midnight. Neither hypothalamic thyrotropin-releasing hormone concentrations nor serum thyroid hormone levels were affected by pinealectomy. Melatonin injected intravenously (1 and 10 mg/kg) or intracerebroventricularly (5 and 50 microgram/rat) had no effect on the basal or cold-stimulated TSH levels, neither was the thyrotropin-releasing hormone induced (50 and 125 ng/rat i.p.) TSH response modified by melatonin (1 mg/kg i.v.). Arginine vasotocin (1 and 100 ng/rat) given intracerebroventricularly had no effect on the basal or cold-stimulated TSH secretion. These results suggest that the pineal has no influence on the basal activity of the hypothalamus-pituitary-thyroid system, but it seems that the cold-induced TSH response depends to a considerable degree on the intact pineal gland.
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PMID:Studies on the role of the pineal gland in the regulation of TSH secretion in postpuberal male rats. 679 Apr 3

Groups of 6-8 male Wistar Olac SPF rats weighing about 300 g were subjected to unforced restriction (UR) in small cages with a metallic bottom and a Plexiglas cover for various intervals from 2 min to 72 h. An acute activation of the pituitary-thyroid axis was found which was manifested by an increase of thyrotropin (TSH) and thyroxine (T4) levels at 2-5 min of UR. This was presumably due to the emotional effect of a rapid transfer and to the placing of the animals into restriction cages. Later, between 3 and 6 h of UR, another, and more pronounced period of activation of the pituitary-thyroid axis and of the peripheral thyroid hormone metabolism was repeatedly observed which lasted until about 36-48 h and was manifested by a highly significant increase of TSH, T4, 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) levels. It was concluded that this phenomenon presumably may be a component of nonshivering thermogenesis resulting from a decreased muscular activity and resembling the conditions occurring under cold stress. Such a view was supported by findings of highly increased nonesterified fatty acid levels in plasma in restricted animals, by unchanged levels of TSH and thyroid hormones found in unrestricted animals kept individually in regular group cages and, finally, by a preventive effect of ambient temperature of 32 degrees C on the pituitary-thyroid activation at 6 h of UR. In some experiments, no substantial differences in hormone levels were found between the animals kept in Plexiglas or stainless wire-mesh restriction cages. Finally, a multifold increase of prolactin level in plasma was found as early as 2 min of UR, the peak being observed between 5 and 20 min and a decrease to about the initial level at about 360 min.
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PMID:Acute and transient activation of pituitary-thyroid axis during unforced restriction in rats: component of nonshivering thermogenesis in conscious animals? 684 Jun 69

Pharmacologic doses of thyroid hormones were administered chronically in diets and acutely by injection to determine their metabolic effects on the development of obesity and the response to cold stress in genetically obese mice. Feeding a 0.1% thyroid powder (TP) diet for 6 weeks to weanling male mice resulted in a marked reduction in weight gain and high mortality in obese but not in non-obese mice. Diets containing 0.01 and 0.02% TP also produced enhanced effects in obese mice during a 13-week feeding period as indicated by reduced body weight, fat and protein and reduced blood glucose at ambient temperature. Both acute and chronic treatment with thyroid hormone produced similar effects in the cold (4 degrees). Blood glucose concentrations were reduced in both obese and non-obese mice, but blood free fatty acid values were unchanged due to hormone treatment. Neither acute nor chronic treatment with thyroid hormones prolonged survival of obese mice during cold exposure. These results suggest a normal or enhanced fat mobilization and utilization in response to exogenous thyroid hormone at ambient temperature. However, the defect in utilization of energy stores for thermogenesis during cold exposure was not ameliorated by this treatment.
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PMID:Influence of thyroid hormone treatment on growth, body composition and metabolism during cold stress in genetically obese mice. 698 55

Male and female rats were fed standard laboratory chow or a highly palatable diet (cafeteria diet) for 10 wk. The cafeteria diet caused an increase in caloric intake and in body weight, and it induced thermogenesis that was associated with elevated plasma triiodothyronine (T3) levels, increased brown adipose tissue size, and enhanced metabolic response to norepinephrine. For a comparable caloric intake, body-weight gain was significantly greater in female than in male rats possibly because of difference in thermogenesis as suggested by the response to norepinephrine. Exercise training (swimming 2 h/day for 10 wk) reduced food intake and body-weight gain and failed to increase norepinephrine-induced thermogenesis in rats fed laboratory chow. In animals fed the cafeteria diet, food intake and body-weight gain were also reduced by exercise training, which at the same time diminished the diet-induced thermogenesis as evidenced by the diminution of 1) brown fat hypertrophy, 2) the elevation of plasma T3, and 3) the hyperthermic response to injected norepinephrine. It is suggested that the thyroid hormone and catecholamines through their actions on the brown adipose tissue are the important regulatory of thermogenesis. Exercise training would reduce the diet-induced thermogenesis by preventing increased T3 production. Enhanced thermogenesis may be considered an adaptive reaction as it serves to reduce fat deposition in animals fed cafeteria diet and to promote nonshivering heat production in the cold. On the other hand, exercise training reduces thermogenesis and thus prevents energy wasting.
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PMID:Effect of diet and exercise on norepinephrine-induced thermogenesis in male and female rats. 706 71

The reported failure of serum TSH to rise in response to the low serum T3 of severe systemic illness may be due to the known stress inhibition of TSH secretion. We therefore measured TSH and total and free thyroid hormones during the course of recovery from severe illness. During recovery, TSH increased at a time when T3 was rising but still below normal (mean TSH during recovery, 6.5 +/- 0.8 SEM microU/ml, n = 41 vs. normal, 2.5 +/- 0.2 SEM microU/ml; n = 31; P less than 0.001), TSH concentrations were negatively correlated with total and free T3 and less strongly correlated with total T4 but not with free T4. Average TSH concentrations were also significantly elevated in severely ill patients with hypothermia that was unrelated to cold exposure (mean TSH, 5.6 +/- 1.3 microU/ml; n = 11; P less than 0.005). The T3 concentrations in these sera were lower than those of other severely ill patients. Thus, during recovery from severe illness and during hypothermia not induced by cold, the relationship between serum T3 and TSH is qualitatively similar to that seen in primary hypothyroidism and may imply a pituitary response to a deficiency of thyroid hormone.
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PMID:The relationship between serum triiodothyronine and thyrotropin during systemic illness. 707 98


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