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)

Diabetes was induced in rats by an intravenous injection of streptozotocin (65 mg/kg body wt), and animals were killed 8 wk later. Some animals were maintained in a diabetic state for 6 wk and then given 2 wk of insulin treatment in vivo. Myofibrils were isolated and ATPase activities measured. Mg2+-ATPase and Ca2+-stimulated ATPase activities were depressed in diabetic rat hearts in comparison to control; insulin treatment normalized these activities. The depression in myofibrillar ATPases was of gradual onset as no changes were detected 2 wk after inducing diabetes. Treatment of diabetic animals with thyroid hormone did not restore changes in myofibrillar ATPase activities. Marker enzyme activities did not reveal any detectable contamination by cardiac membranes. Mg2+-ATPase activity of myofibrillar preparations from control and diabetic hearts responded differently to N-ethylmaleimide modification. Furthermore, myofibrillar sulfhydryl reactivity to 5,5'-dithiobis(2-nitrobenzoic acid) was significantly depressed in diabetic preparations in comparison to control and insulin-treated diabetic animals. These results suggest that the defect in myofibrillar ATPase activities in chronic diabetes may be due to some modification of sulfhydryl groups.
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PMID:Mechanisms of the defect in cardiac myofibrillar function during diabetes. 315 18

Two patients with depression that was refractory to tricyclic antidepressant therapy alone and in combination with lithium or triiodothyronine (T3) were treated with the monoamine oxidase inhibitor phenelzine. In both cases, the addition of T3 potentiated the antidepressant response to phenelzine. These observations suggest that thyroid hormone potentiation may not be specific to one class of antidepressant drugs.
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PMID:Triiodothyronine potentiation of the antidepressant effect of phenelzine. 317 Apr 93

Assessment of metabolic rate was useful in evaluating refractory depression in six of 15 women. Five of the six had normal levels of T3 and T4; however, each had an elevated thyrotropin-stimulating hormone level or a low metabolic rate. The depressions responded to medication with thyroid hormone.
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PMID:Occult thyroid dysfunction in patients with refractory depression. 339 53

Observations on the effect of thyroid hormones on mouse submaxillary gland epidermal growth factor (EGF) and on the complementary effect of EGF on cultured thyroid cells led us to examine the interaction between EGF and thyroid hormones in the whole animal, during and after 24 h of infusion of 3.3 micrograms/kg X h mouse EGF into 6 merino ewes. There was a profound depression of both circulating T4 and T3 levels, to less than 20% of saline-infused control values, extending beyond the end of infusion. Plasma TSH concentrations were unchanged during the first 8 h of the infusion, excluding the likelihood of a suppressive effect of EGF on the hypothalamic-pituitary axis. Serum rT3 and 3,3'-diiodothyronine, however, experienced a more transitory 6-fold increase. These findings are consistent with a dual inhibitory effect of EGF on both thyroid hormone secretion and peripheral metabolism.
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PMID:Epidermal growth factor: effect on circulating thyroid hormone levels in sheep. 348 43

Due to the lately increased oral nitrate intake of humans and animals the influence of 3% KNO3 in the diet on growth and the thyroid hormone and somatomedin-C-concentration in the serum was to be tested in an experiment with growing pigs in case of different iodine supply. The investigations were undertaken in 3 groups with 9 piglets each. The animals were 6 weeks old: 1. nitrate-exposed, 2. pair-fed to group 1 (without nitrate), 3. ad libitum without nitrate. The mean daily weight gains amounted to 242, 274 and 393 g respectively, after a five-week test period. Compared to the ad libitum control group, the T4-, T3-, rT3- and Sm-C-level of nitrate-exposed animals was significantly lower after 5 weeks. There were no statistically relevant differences between nitrate-exposed and pair-fed animals with regard to the T3- and Sm-C-level. After the 5-week test period with an iodine supply covering the requirement the rations of all 3 groups were supplemented with further 0.8 mg iodine/kg. The T4-, T3- and rT3-levels of the animals of group 1 normalized within one week. The Sm-C-levels of the nitrate-exposed and pair-fed group were still decreased. The investigations show that an increased nitrate intake via food and drinking water influences the thyroid hormone metabolism. It should be taken into consideration in the etiology of endemic struma. Furthermore, excessive nitrate intakes influence the Sm-C-concentration and thus growth due to food intake depression.
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PMID:Effect of chronic dietary nitrate and different iodine supply on porcine thyroid function, somatomedin-C-level and growth. 355 13

The relationship between thyroid disorders and depression is well known. This type of endocrine disease is mainly observed in patients with depression resistant to appropriate antidepressor therapy. Three clinical forms of this association may be distinguished: hypothyroidism in a patient with depression but without a previous psychiatric history; a relapse of depression in a manico depressive patient who has developed hypothyroidism; the finding of slight thyroid dysfunction (increased TSH response after injection of TRH) in a patient with depression. The frequency of the association of hypothyroidism and resistant depression underlines the need to perform thyroid function tests in all depressed patients who do not respond normally to appropriate antidepressor therapy. The precise mechanism of the resistance of depressive symptoms to tricyclic antidepressors is unclear. Several arguments point to an effect of triiodothyronine on central noradrenergic receptors. In practice, significant hypothyroidism implies substitute therapy. Minor thyroid dysfunction (abnormal TRH test alone) may require the association of tricyclic antidepressors and thyroid hormone although the indications and precise dosages of this drug association have not been established.
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PMID:[Depressions resistant to tricyclic antidepressive treatment and hypothyroidism]. 357 93

The effects of thyroid state on the respiration of the isolated heart were investigated using retrograde perfused rat and guinea pig hearts. In both species, hypothyroidism caused a marked depression in circulating thyroid hormone concentrations and in the respiration of the isolated, retrograde perfused heart. The effects on myocardial respiration could be attributed to changes in the contraction frequency and in the oxygen consumption per beat, with little contribution from basal respiration. Treatment of animals with thyroxine elevated plasma thyroid hormones to a similar extent in rats and guinea pigs. In the latter, thyroxine treatment was associated with substantial increases in the contraction frequency and the oxygen consumption per beat of the isolated heart. In contrast, only small changes were apparent in the retrograde perfused rat heart, observations that were confirmed in rat hearts perfused at near physiological work loads. It was concluded that rat hearts isolated from normal animals function at near maximal thyroid state, in contrast to the guinea pig heart, which requires higher circulating concentrations of thyroid hormones to attain maximal responses.
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PMID:Effects of thyroid state on respiration of perfused rat and guinea pig hearts. 363 Dec 89

Depressed thyroid hormone levels are commonly found in sick patients. Low serum testosterone concentrations have also been described in men suffering from a number of illnesses. To investigate whether this might be a non-specific marker of illness, various endocrine parameters were measured in 30 male patients in a general medical ward. Patients were suffering from a wide spectrum of medical disorders and were not receiving drugs known to affect endocrine function. Results were compared with a healthy age-matched control group. Serum testosterone concentrations (mean +/- SE) were low in the patient group (8.9 +/- 1.1 vs. 18.2 +/- 1.4 nmol/l, p less than 0.001), correlated significantly with serum T3 levels but were not related to prognosis. Half the patients had testosterone levels below the normal control range. Changes in testosterone concentrations could not be explained on the basis of binding protein changes, hyperprolactinaemia or depressed pituitary secretion of gonadotrophins. Depression of serum testosterone concentrations is a non-specific marker of illness.
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PMID:Male hypogonadism--a non-specific consequence of illness. 367 64

Night-time pineal levels of tryptophan, 5-hydroxytryptophan, serotonin, N-acetylserotonin, melatonin, 5-hydroxyindoleacetic acid and the activities of the two enzymes N-acetyltransferase and hydroxyindole-O-methyltransferase involved in the cyclic production of melatonin were determined in male albino rats and Syrian hamsters that were implanted with thyroxine or thyroidectomized two weeks earlier. Both treatments depressed nocturnal pineal melatonin content in rats and hamsters. The cause of this depression is not known, although minor alterations in the substrates and the enzymes involved in melatonin production were observed. The data suggest that alterations in thyroid hormone levels may increase the release of nocturnal melatonin from the pineal, thereby allowing less to accumulate in the gland.
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PMID:Hormonal modulation of cyclic melatonin production in the pineal gland of rats and Syrian hamsters: effects of thyroidectomy or thyroxine implant. 391 2

We have previously reported that 5,5'-diphenylhydantoin (DPH) inhibits total cellular and specific nuclear T3 binding by cultured GC cells, a rat pituitary tumor cell line that produces GH. DPH decreased competitively the rate of T3 accumulation by GC cells and noncompetitively inhibited specific nuclear T3 binding as well. To determine the biological consequences of these DPH effects on cellular and nuclear T3 binding, we studied the effect of DPH on the growth rate and GH production of GC cells cultured in Dulbecco's Modified Eagle's Medium with 10% serum. Incubation with T3 stimulated the GC cell growth rate in a dose-dependent manner. The half-maximal growth rate was achieved at a T3 concentration of 0.18 nM, and the maximal effect was observed at 0.4 nM T3. Addition of DPH to GC cells cultured with 0.15 nM T3 resulted in a dose-dependent decrease in the GC cell growth rate. The half-maximal depression of the rate of GC cell growth occurred at 185 microM DPH, a concentration that results in an approximately 50% decrease in cellular and nuclear T3. The DPH-induced decrease in GC cell growth was abolished by the addition of increasing concentrations of T3 (maximal concentration, 1.0 nM). Similarly, DPH effected a dose-dependent decrease in GH production in cells cultured with physiological concentrations of T3 (0.15 nM). The decrease in GH production of cells incubated with 200 microM DPH was associated with a decrease of similar magnitude in GH mRNA. These findings suggested that the DPH effect on GH production was mediated at a pretranslational level. Addition of increasing concentrations of T3 up to 5 nM completely abolished the DPH-associated decrease in GH production. Finally, studies of the effects of DPH on cell growth and GH production in cultures maintained with T3-depleted conditions were carried out to detect putative agonist activity of DPH. In the present investigation, we were unable to detect agonist activity of DPH that was more than 10-15% of the effect of maximal doses of T3. The data suggest that DPH attenuates the action of T3 in GC cells, probably because of a decrease in the steady state concentrations of cellular and nuclear T3. These attributes of DPH suggest that the drug or related analogs may serve as prototypes of agents that may decrease thyroid hormone activity at target tissues.
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PMID:5,5'-Diphenylhydantoin (phenytoin) attenuates the action of 3,5,3'-triiodo-L-thyronine in cultured GC cells. 399 15


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