Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in serum total thyroxine concentration (TT4) and the effects of thyroxine (T4) and 3,5,3'-triiodothyronine (T3) injection on plasma free fatty acid (FFA) level and rectal temperature (Tre) responses were measured in six dogs at rest and during 1 h of submaximal treadmill exercise. At rest there were no increases in FFA level or Tre up to 72 h after thyroid hormone treatment. During exercise, 5 h after a single T4 injection (0.1 mg/kg), there was a) a significant increase in TT4, although the resting level was markedly elevated, and b) a significant increase in FFA concentration and Tre above control values. Seventy-two hours after T4 injection there was a similar increase in TT4 during exercise and both FFA and Tre levels were greater than 5-h values. The elevated Tre was not associated with increased plasma Na+, K+, or osmotic concentrations. Compared with T4 data, T3 injection (0.1 mg/kg) resulted in greater increases in FFA level and Tre during exercise; two animals reached 43.1 degrees C. There were no significant differences in the respiratory exchange ratio (R) or O2 uptake between the control and T3 experiments. It was concluded that thyroid hormones markedly enhance FFA mobilization and elevated Tre during exercise, but not a rest. The hyperthermic response appears to be due to an increase in the level of regulated body temperature rather than to a depression of heat dissipation.
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PMID:Thyroid hormone-induced changes in body temperature and metabolism during exercise in dogs. 116 55

The effect of short-term dexamethasone administration (8 mg daily for 3 days) on thyroid hormone response to exogenous TSH (bovine TSH, 5 IU i.m.) was studied in 16 euthyroid volunteers. Serum T3 and T4 concentrations were measured by radio-immunoassay prior to and 2, 6, 12, 24, and 49 hr after bTSH injection, both under basal conditions and during dexamethasone treatment. In all subjects bTSH administration raised both T3 and T4 concentrations significantly. Dexamethasone treatment induced a slight depression of endogenous TSH (m +/- SEM = 2.0 +/- 0.4 versus 1.6 +/- 0.3 muU/ml) and T4 (6.8 +/- 0.4 versus 6.1 +/- 0.2 mug/100 ml) basal values and a significant decrease in T3 value (1.16 +/- 0.09 versus 0.64 +/- 0.06 ng/ml, p = 0.005). The mean increment of both T3 and T4 after bTSH injection was percentually unchanged during dexamethasone treatment but, due to lowered basal value, T3 levels at each time interval after TSH + dexamethasone were significantly lower than the corresponding values observed after TSH alone. The present data show that high dexamethasone doses decrease T3 serum levels significantly without inhibiting T3 response to TSH stimulation. Only a slight lowering was observed in T4 levels.
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PMID:Effect of dexamethasone on thyroid hormone response to TSH. 118 94

Thyroidal radioiodine release increased shortly after a single injection of small doses of PTU, while moderate doses of MMI produced a similar increase of thyroidal radioiodine release with a latency of 7-9 hr. Large doses of PTU and MMI failed to augment thyroidal radioiodine release for at least 29 to 34 hr after the initial administration of goitrogens, although plasma TSH increased significantly because of goitrogen administration. An increase of thyroid hormone release in response to exogenous TSH was depressed by PTU and MMI in rats and mice treated with T4. Since this depression of TSH action only continued for a short period in spite of continuous administration of goitrogens, and since final thyroidal radioiodine release rate was similar to that produced by small doses of PTU, the effects mentioned were not simply due to general toxic action of goitrogens. It is suggested that large doses of PTU and MMI not only block thyroid hormone synthesis but also interfere with the action of TSH on thyroid hormone secretion.
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PMID:Inhibitory effect of large doses of propylthiouracil and methimazole on an increase of thyroid radioiodine release in response to thyrotropin. 126 85

We assessed the effect of treatment with the tricyclic antidepressant, desipramine, on peripheral thyroid hormone levels in 28 severely depressed patients. Only those whose depression responded showed a decrease in their thyroxine levels without alteration of other thyroid function tests. In a second study involving 38 depressed patients, we observed an increased response to antidepressant treatment with the addition of triiodothyronine but not equivalent doses of thyroxine (T4). The finding is consistent with the decreases in plasma T4 levels which accompany an antidepressant response to desipramine.
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PMID:Antidepressants and thyroid hormone levels. 151 66

To examine the signals regulating cardiac growth and molecular structure of subcellular organelles, cardiac hypertrophy was induced in rats by constriction of the abdominal aorta for 12-13 wk or by treatment with a carnitine palmitoyltransferase I inhibitor, etomoxir (12-15 mg/kg body wt) for 12-13 wk. In contrast to pressure overload, etomoxir redistributed the myosin isozyme population from V3 to V1 and increased the sarcoplasmic reticulum (SR) Ca(2+)-stimulated ATPase activity. When rats with pressure-overloaded hearts were treated with etomoxir, the cardiac hypertrophy was increased whereas the shift in myosin isozymes from V1 to V3 was prevented and the depression in SR Ca(2+)-stimulated ATPase activity was reversed. Plasma thyroid hormone and insulin concentrations were not altered but triglyceride concentrations were reduced in etomoxir-treated rats with pressure overload. The data demonstrate a dissociation between cardiac muscle growth and changes in subcellular organelles and indicate that a shift in myocardial substrate utilization may represent an important signal for molecular remodeling of the heart.
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PMID:Modification of subcellular organelles in pressure-overloaded heart by etomoxir, a carnitine palmitoyltransferase I inhibitor. 153 68

The genetically epileptic-prone rat (GEPR) is a valuable model for the study of gene-linked abnormalities involved in epilepsy. In comparison with normal Sprague-Dawley controls, we found, in GEPRs, a marked depression in local cerebral glucose utilization, widespread throughout the brain. This depression was accompanied by a significant increase of blood-brain barrier permeability and a reduction in regional blood volume. Finally GEPRs showed lower plasma levels of total triiodothyronine than normal controls. One can speculate that alterations in cerebral metabolism and microvascular regulation and thyroid hormone imbalance may be gene-linked factors involved in seizure susceptibility.
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PMID:Evaluation of local cerebral glucose utilization and the permeability of the blood-brain barrier in the genetically epilepsy-prone rat. 154 51

Free thyroxine index (FT4I), serum thyroxine (T4) and thyrotrophin concentrations were measured in 45 depressed subjects and 23 controls. The FT4I am/pm ratio was significantly higher in depressed subjects than in controls. This elevated diurnal ratio of thyroid hormones in depression adds to the literature on the chronobiology of affective disorders, and may help to explain differences in thyroid hormone levels in depressed patients in other studies, where time of sampling has seldom been reported.
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PMID:Diurnal profiles of thyroid hormones are altered in depression. 154 41

Several studies that have examined heterogeneous groups of patients suggest that altered thyroid function may distinguish melancholic from nonmelancholic depression. We therefore measured basal thyroid hormone levels in 90 unipolar depressed patients who were divided into melancholic and nonmelancholic subgroups according to three definitions. Levels of thyroxine, triiodothyronine, and thyrotropin, obtained using an ultrasensitive assay, did not distinguish the subtypes of depression. However, severity of depression contributed significantly to the difference between these subtypes according to DSM-III and Research Diagnostic Criteria.
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PMID:The thyroid and melancholia. 160 83

Although the psychological disturbances accompanying Graves' disease are well known, the time required for normalisation of these disturbances during antithyroid drug treatment is not known. Therefore sequential psychological testing during the course of Graves' disease was done. There are also contradictory results concerning the possible correlation of neurophysiological and psychological test results during the course of Graves' disease with thyroid hormone values. Finally, psychological disturbances have been proposed as possible etiologic factors in Graves' disease. In our study, a significant decrease in anxiety and irritability could be observed at the time euthyroidism was achieved. Self-evaluations of depressivity, activity, exhaustion, well-being, extraversion, introversion, and the ability to concentrate changed 1 or 2 months after euthyroidism was induced. Similar test results could be observed after induction of euthyroidism by antithyroid drugs and subtotal thyroid resection. Therefore the mode of therapy does not seem to influence the course of normalisation of psychological parameters. In contrast to other investigations there was hardly any correlation between thyroid hormone values and psychological test results or the ability to concentrate. Nontheless, patients with Graves' disease showing high scores for depression and anxiety exhibit abnormal peripheral helper/suppressor T-lymphocyte relations. Furthermore, patients suffering from Graves' disease tend to be more anxious than controls. It remains to be determined whether an increased susceptibility to psychological disturbances has led to these alterations of lymphocyte subsets in Graves' disease patients with severe depression and anxiety.
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PMID:Sequential psychological testing during the course of autoimmune hyperthyroidism. 170 Jan 85

The influence of hypothyroidism on the transport of phosphate and on the lipid composition in rat-liver mitochondria was examined. It was found that the rate of phosphate transport is reduced (around 40%) in mitochondria from hypothyroid rats compared to that obtained in mitochondria from normal rats. Treatment of hypothyroid rats with thyroid hormone reverses this effect completely. Kinetic analysis of the phosphate transport indicates that only the Vmax of this process is affected, while there is no change in the Km values. The lower rate of phosphate transport in mitochondria from hypothyroid rats is also demonstrated by swelling experiments. There is no significant difference either in the respiratory control ratios or in the ADP/O ratios between these two types of mitochondria. The hepatic mitochondrial lipid composition is altered significantly in hypothyroid rats. The total cholesterol increases, the phospholipids decrease and the cholesterol/phospholipid molar ratio increases (around 40%). Among the phospholipids, cardiolipin shows the greatest alteration (30% decrease in the hypothyroid rats). The phosphatidylethanolamine/phosphatidylcholine ratio also decreases. Alterations were also found in the pattern of fatty acids. These changes in lipid composition may be responsible, at least in part, for the depression of the phosphate carrier activity in mitochondria from hypothyroid rats.
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PMID:The influence of hypothyroidism on the transport of phosphate and on the lipid composition in rat-liver mitochondria. 175 24


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