Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were made hypo and 'hyperthyroid' with propylthiouracil (PTU) and L-Thyroxine (L-T) respectively. The hypo and hyperthyroid status in these rats were confirmed by serum level of T4 and T3. Liver iron was significantly increased in both the hypo and hyperthyroid animals. However, liver ferritin synthesis rate was reduced by 36% in hypothyroid rats, and elevated by 38% in hyperthyroid ones. A similar trend was seen in liver ferritin concentration. Further, serum transaminases were elevated only in animals of the hyperthyroid group. It appears from the present data that ferritin metabolism is influenced by thyroid hormone as well as by iron. Thus, the raised serum ferritin in hyperthyroid patients may be partially attributed to increased ferritin synthesis in the liver and its possible leakage into circulation.
 ...
PMID:Relation between thyroid status and ferritin metabolism in rats. 128 38

Tiratricol has been used to suppress pituitary TSH secretion, with reported attenuation of extrapituitary thyromimetic effects. A randomized, double-blind trial was performed to define precisely the tissue-specific thyromimetic actions of tiratricol. Ten athyreotic patients, treated for thyroid carcinoma, were randomly assigned to receive L-T4 sodium 0.7 micrograms/kg daily and either tiratricol 10 micrograms/kg or placebo twice daily. The daily dose of L-T4 was increased by 25-50 micrograms increments until the TRH-stimulated TSH level was less than 0.1 mU/L. After measurement of biochemical and physiological parameters of thyroid hormone actions, patients crossed treatment groups. Patients required 46% less L-T4 to achieve equivalent TSH suppression when taking tiratricol. Hepatic effects were enhanced by tiratricol administration, with significant increases in sex hormone binding globulin and ferritin concentrations, 14% and 37%, respectively. Levels of serum cholesterol, LDL cholesterol, and apolipoprotein B were reduced by 7%, 10%, and 13%, respectively, during tiratricol therapy. Triglyceride levels also declined, but there were no changes of high density lipoprotein cholesterol or apolipoproteins AI and AII. Resting metabolic rate, body weight, urea nitrogen excretion, and symptoms did not differ between the two treatment regimens. Cardiovascular function, as reflected by mean arterial pressure and pulse wave arrival time, was not different during tiratricol therapy. Skeletal metabolic activity was affected by tiratricol, with marked elevation of osteocalcin without significant change in serum calcium, PTH, and urinary calcium and hydroxyproline excretion. Tiratricol has increased hepatic and skeletal actions of potential therapeutic value, but does not have enhanced thyromimetic activity specific to the pituitary gland.
 ...
PMID:Organ-specific effects of tiratricol: a thyroid hormone analog with hepatic, not pituitary, superagonist effects. 151 83

TSH secretion, with particular regard to the nocturnal surge of the hormone, was evaluated in 15 women (age range, 35-66 yr; mean, 50 yr) with untreated major endogenous depression and 15 healthy women (age range, 32-67 yr; mean, 53 yr) using an ultrasensitive assay. Mean morning (0830 h) TSH values did not differ in the 2 groups (1.3 +/- 02 mU/L in depressives and 1.4 +/- 0.1 mU/L in controls), whereas mean nighttime (2400-0200 h) values were significantly reduced in depressives (1.5 +/- 0.3 vs. 3.1 +/- 0.3 mU/L; P less than 0.0005). At variance with the control group, morning and nighttime TSH values did not differ in the depressives. The nocturnal serum TSH surge was abolished in 14 of 15 depressed patients. The mean peak TSH value after TRH was slightly yet significantly lower in the depressives. Patients with subnormal (less than 0.4 mU/L) TSH values in the morning had a serum TSH increase after TRH less than 2 mU/L in 5 of 6 cases and a lack of the nocturnal TSH surge in 6 of 6. Among the 9 patients with normal TSH values in the morning, the nocturnal serum TSH surge was lost in 8 of 9, whereas the response to TRH was normal in all. The depressives, at variance with other reports, showed significantly lower values of total and free thyroid hormones. Mean serum sex hormone-binding globulin (SHBG) and ferritin were also significantly reduced. In conclusion, major endogenous depression is associated with a major impairment of TSH secretion, which baseline TSH measurements in the morning and the evaluation of the TSH response to TRH may not reveal. In this regard, the loss of the nocturnal serum TSH rise would appear to be a more sensitive indicator of hypothalamus-pituitary-thyroid axis alterations in depressives than the TRH test, which is commonly used in the evaluation of these patients. The lack of the nocturnal TSH surge may be responsible for the reduced thyroid hormone secretion and supports the case for some degree of central hypothyroidism in endogenous depression.
 ...
PMID:Nocturnal serum thyrotropin (TSH) surge and the TSH response to TSH-releasing hormone: dissociated behavior in untreated depressives. 211 39

We investigated iron metabolism in 47 women with thyrotoxic Graves' disease. Serum iron, ferritin, transferrin, triiodothyronine and thyroxine concentrations were RIA measured before and after methimazole treatment when patients became euthyroid. The control group consisted of 52 healthy women. We noted that serum ferritin levels and the ferritin to transferrin ration were significantly lower while the iron to ferritin ratio was higher in patients before and after methimazole therapy. Iron concentration as well as the iron to transferrin and the iron to thyroid hormone ratios were decreased only before treatment.
 ...
PMID:Serum ferritin, iron and transferrin in women with thyrotoxic Graves' disease before and after methimazole treatment. 213 11

Physiological responses at 16 degrees C were studied in 11 women, age 28 +/- 2(mean +/- S.E.) years and 26 +/- 2% fat, after their body iron stores were depleted by diet (5.0 mg iron x 2,000 kcal-1 x d-1), phlebotomy and menstruation for about 80 d and were repleted by diet (13.7 mg iron x 2,000 kcal-1 x d-1) for about 100 d, including daily iron supplementation (50 mg of iron as ferrous sulfate) for the last 14 d of repletion. Iron depletion was characterized by a decline (p less than 0.05) in hemoglobin (12.0 +/- 0.2 g x dl-1), ferritin (5.5 +/- 0.5 ng x ml-1) and body iron balance (-9.1 +/- 2.6 mg x 6 d-1). Iron repletion, including supplementation, increased (p less than 0.05) hemoglobin (12.6 +/- 0.1 g x dl-1), ferritin (9.5 +/- 0.4 ng x ml-1) and iron balance (+67 +/- 6.7 mg x 6 d-1). Iron depletion reduced (p less than 0.05) metabolic heat production (49.6 +/- 1.1 vs 53.6 +/- 1.2 W x m-2) during acute cold exposure. The rates of cooling of the core and periphery were greater (p less than 0.05) during iron depletion than repletion. A shift in the lower core temperature threshold for shivering was paralleled by an earlier onset of shivering (p less than 0.05) in iron depletion indicating an adaptation in cold tolerance in an attempt to maintain core temperature. Iron depletion was associated with blunted post-exposure increases in plasma thyroid hormone concentrations and greater (p less than 0.05) increases in plasma norepinephrine concentrations as compared to iron repletion. In a subsample of the women, no significant effect of calcium or ascorbic acid supplementation was found on responses to cold exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Thermogenesis and thermoregulatory function of iron-deficient women without anemia. 224 32

In a pilot therapeutic trial, four patients with amyotrophic lateral sclerosis (ALS) were treated with long term, continuous infusions of TRH, three intrathecally and one epidurally. They had prompt increases in serum TSH and thyroid hormone concentrations, averaging 120% for TSH, 49% for serum T4, 68% for the serum free T4 index, 49% for serum T3, and 67% for the serum free T3 index. These elevations were statistically significant for all but serum T3 and persisted for the duration of treatment (4-7 months). Mean values during treatment were near the upper limit of normal for each of these hormone measurements. After TRH withdrawal, serum TSH fell transiently below the normal range. A comparison group of four patients with ALS treated by twice weekly intrathecal bolus doses of TRH had no significant changes in serum TSH, T4, or T3. During continuous TRH treatment, the responsiveness of both TSH and PRL to a standard iv TRH stimulation test was blunted, but not abolished. Basal serum PRL was occasionally elevated in the two women during continuous TRH treatment, but was normal in the men, and serum GH was normal in all patients. In the patients receiving continuous TRH treatment, indexes of end-organ effects of thyroid hormone were inconclusive; none had a rise in serum ferritin, one of four had a rise in serum sex hormone-binding globulin, and three had increased creatinuria. These results provide direct evidence in man that chronic TRH administration can cause modest sustained increases in serum TSH and thyroid hormones, though the metabolic consequences of these changes are uncertain, and appears to raise the set-point of the pituitary-thyroid axis, i.e. the serum T4 and T3 concentrations needed for a given degree of suppression of basal TSH secretion.
 ...
PMID:Sustained rises in serum thyrotropin, thyroxine, and triiodothyronine during long term, continuous thyrotropin-releasing hormone treatment in patients with amyotrophic lateral sclerosis. 309 28

Insurers, employers, and individuals create demands for laboratory testing in "wellness programs." Tests chosen to identify cases deserving intervention included routine automated chemical tests plus high-density lipoprotein cholesterol, ferritin, and thyroid tests. Participants' unwarranted concerns were addressed with a personalized reporting schema. We tested 1338 individuals, identified 224 (16.7%) with significant abnormalities, and made phone contact follow-up with 193 (86%) of these six to 14 months later. Cholesterol results suggesting increased risk of heart disease were frequent, and were not studied. Interventions were initiated in 55 of the 193 followup cases (49 by physician and six by participants), including prescription of iron or thyroid hormone, counseling on dietary or alcohol intake, and repeat testing. For 58, there was medical advice without intervention; abnormal results were ignored by 79. Noteworthy participant anxiety was manifested in two of the 193 cases, both of whom were treated with iron. We conclude that 4% of the original 1338 participants potentially benefitted from intervention. Ferritin and thyroid tests initiated 33 (61%) of these 55 specific therapeutic interventions.
 ...
PMID:Chemistry profiles in "wellness programs": test selection and participant outcomes. 339 Sep 15

Serum ferritin measurements were evaluated as a marker of thyroid hormone action on peripheral tissues. Mean serum ferritin concentrations were not significantly different in euthyroid, thyrotoxic, and hypothyroid subjects due to a wide spread in ferritin levels among individuals. Intraindividual changes in serum ferritin, however, occurred with changing thyroid function. All 18 patients with thyrotoxic Graves' disease had a decrease in serum ferritin levels when they became euthyroid during antithyroid drug therapy. Furthermore, a significant intraindividual correlation between serum levels of ferritin and T4 or T3 was found in 2 patients with thyrotoxic Graves' disease in whom levels were measured serially throughout the course of therapy. Similarly, serum ferritin levels increased in all 12 hypothyroid patients with Hashimoto's disease when euthyroidism was achieved with L-T4 therapy. Administration of 75 micrograms T3 daily for 1 week to 11 euthyroid subjects resulted in a 23-243% (mean +/- SD, 117 +/- 70%) increase in serum ferritin above basal values. In contrast, in 3 patients with thyroid hormone resistance, the same treatment produced rises in serum ferritin concentrations of only 2%, 5%, and 15%. Our data suggest that alterations in thyroid status in a given individual produce changes in serum ferritin levels. Measurement of this protein before and after T3 therapy may prove useful in the diagnosis of thyroid hormone resistance.
 ...
PMID:Serum ferritin as a marker of thyroid hormone action on peripheral tissues. 403 Oct 12

The common occurrence of increased serum PBI concentration in patients with lysinuric protein intolerance (LPI) was elucidated by further studies. The reason was found to be an increase in the concentration of thyroid binding globulin (TBG), concomitantly with an increase in the binding capacity of TBG. The concentrations of serum thyroxine and triiodothyronine were elevated, whereas the free thyroxine index remained normal. The free triiodothyronine index was slightly increased. The binding capacity of thyroid hormone binding pre-albumin (TBPA) was significantly decreased. The concentrations of reverse triiodothyronine (3,3',5'-T3) and of 3,3'-diiodothyronine were normal. In all patients serum lactic acid dehydrogenase activities and ferritin concentrations were elevated. The reason for the almost constant increase in TBG remains obscure. It may be related to the primary disorder of LPI, a defect in diaminoacid transport.
 ...
PMID:Increase in thyroxine-binding globulin (TBG) in lysinuric protein intolerance. 678 26

The cytoplasmic iron regulatory protein (IRP) modulates iron homeostasis by binding to iron-responsive elements (IREs) in the transferrin receptor and ferritin mRNAs to coordinately regulate transferrin receptor mRNA stability and ferritin mRNA translational efficiency, respectively. These studies demonstrate that thyroid hormone (T3) can modulate the binding activity of the IRP to an IRE in vitro and in vivo. T3 augmented an iron-induced reduction in IRP binding activity to a ferritin IRE in RNA electrophoretic mobility shift assays using cytoplasmic extracts from human liver hepatoma (HepG2) cells. Hepatic IRP binding to the ferritin IRE also diminished after in vivo administration of T3 with iron to rats. In transient transfection studies using HepG2 cells and a human ferritin IRE-chloramphenicol acetyltransferase (H-IRE-CAT) construct, T3 augmented an iron-induced increase in CAT activity by approximately 45%. RNase protection analysis showed that this increase in CAT activity was not due to a change in the steady state level of CAT mRNA. Nuclear T3-receptors may be necessary for this T3-induced response, because the effect could not be reproduced by the addition of T3 directly to cytoplasmic extracts and was absent in CV-1 cells which lack T3-receptors. We conclude that T3 can functionally regulate the IRE binding activity of the IRP. These observations provide evidence of a novel mechanism for T3 to up-regulate hepatic ferritin expression, which may in part contribute to the elevated serum ferritin levels seen in hyperthyroidism.
 ...
PMID:Thyroid hormone modulates the interaction between iron regulatory proteins and the ferritin mRNA iron-responsive element. 866 26


1 2 3 Next >>