Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. It was shown that the development of liver glucokinase in the rat coincided with a peak in the levels of circulating thyroid hormone at about the 16th postnatal day. 2. Administration of thyroid inhibitors blocked the development of the enzyme and administration of thyroid hormone restored activity to normal levels. 3. Glucokinase could be induced prematurely as early as the 2nd postnatal day by the administration of thyroid hormone followed by daily injection of glucose (10 mg/g body weight). 4. Glucocorticoids and corticotropin failed to induce glucokinase activity prematurely. 5. The postnatal increase in circulating thyroid hormone levels together with increased intake of carbohydrate at weaning may be the normal physiological stimulus for induction of this enzyme.
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PMID:Premature induction of glucokinase in the neonatal rat by thyroid hormone. 16 49

A 43 year old man with diabetes insipidus who showed panhypopituitarism and marked hypergammaglobulinemia due to histiocytosis X is reported. His low basal plasma adrenocorticotropin (ACTH) and growth hormone (GH) failed to respond to insulin-induced hypoglycemia. His basal serum thyroid hormone level was below normal and normal basal plasma thyrotropin (TSH) showed a delayed response with normal peak value to TSH-releasing hormone (TRH). Normal basal plasma pituitary gonadotropin also showed a delayed response with normal peak value to luteinizing hormone-releasing hormone (LH-RH). Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. These results, combined with diabetes insipidus, suggested that the panhypopituitarism in these patients was hypothalamic in origin. The polyclonal hypergammaglobulinemia was characterized by elevated serum IgG and IgE levels which returned to normal after corticosteroid treatment with concomitant clinical improvement. Elevated serum IgE levels, tissue and peripheral eosinophilia, and the effectiveness of corticosteroid therapy support the hypothesis that some allergic mechanism may be involved in the pathogenesis of this disease.
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PMID:A case of histiocytosis X associated with panhypopituitarism and hyperimmunoglobulinemia G and E. 22 67

Using in situ hybridization histochemistry, we have investigated the effect of thyroid hormone on the expression of several peptide mRNAs in the hypothalamic paraventricular nucleus (PVN) of adult male rats. Hypothyroidism was induced by surgical ablation of the thyroid gland. The animals (control sham-operated, thyroidectomized, thyroidectomized+T4 replaced rats) were studied 28 and 50 days after surgery. Sections of the PVN were hybridized using synthetic oligonucleotide probes complementary to mRNA for thyrotropin-releasing hormone (TRH), corticotropin-releasing hormone (CRH), galanin (GAL), enkephalin (ENK), neurotensin (NT), vasoactive intestinal polypeptide (VIP) and vasopressin (VP). GAL mRNA was also analyzed in the anterior paraventricular, arcuate, and dorsomedial nuclei of the hypothalamus. At the PVN level, a feedback effect of thyroid hormone on TRH synthesis was demonstrated by the TRH mRNA increase in hypothyroidism and by its decrease in hyperthyroidism. Hypothyroidism caused a dramatic decrease in GAL mRNA in parvo- and magnocellular PVN neurons both 28 and 50 days after thyroid ablation, whereas no effect was seen in VP mRNA, the main peptide hormone coexisting with GAL. The T4 replacement prevented the GAL mRNA impairment. Hypothyroidism did not influence GAL mRNA in the anterior PVN, perifornical area or in the arcuate nucleus, whereas a decrease in GAL mRNA was observed in the dorsomedial nucleus. VIP mRNA, which is undetectable in the PVN of normal animals, was present in several PVN neurons after thyroidectomy. CRH mRNA was decreased after thyroidectomy, whereas the T4 restitution caused an upregulation. The levels of ENK or NT mRNA were not significantly affected by the thyroid status. The present results show that, in addition to TRH mRNA, other hypothalamic peptide mRNAs are affected by thyroid hormone levels.
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PMID:Response of hypothalamic peptide mRNAs to thyroidectomy. 128 6

Thyroid hormone and thyrotropin (TSH) levels were evaluated before and after adrenal replacement in eight patients (six men and two women, 35-62 years old) with isolated adrenocorticotropin (ACTH) deficiency. Six patients (cases 1-6) showed TSH excess before treatment. Four patients (cases 1-4), who initially had subnormal thyroid hormone levels, showed resolution of biochemical features of primary hypothyroidism after treatment, although TSH excess has persisted in two patients (cases 1 and 2). Case 1 had an extremely high titer of antimicrosomal antibody (MCHA), and cases 2 and 3 showed histologically and cytologically chronic thyroiditis, despite negative results for MCHA and antithyroglobulin antibody, respectively. Two patients (cases 5 and 6), who had had normal thyroid hormone levels and did not show the significant rise in serum T3 in TSH releasing hormone testing, showed TSH normalization without changes in serum thyroid hormone levels after treatment. The other two patients (cases 7 and 8), who initially had normal TSH and thyroid hormone levels, did not show the significant changes in serum TSH and thyroid hormone levels after treatment. The prevalence of chronic thyroiditis coexistence in isolated ACTH deficiency may be higher than predicted. Therefore, TSH excess before adrenal replacement may be attributed to not only direct enhancement of TSH release due to chronic cortisol deficiency but also to thyroid dysfunction due to chronic thyroiditis. It is possible that hypothyroidism due to chronic thyroiditis can be improved only by adrenal supplementation.
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PMID:Evaluation of thyroid function in patients with isolated adrenocorticotropin deficiency. 133 72

Thyrotropin-releasing hormone (TRH), ovine corticotropin-releasing hormone (oCRH) (both 268 nM), and mammalian gonadotropin-releasing hormone (mGnRH) (268 and 2680 nM) stimulated the secretion of bioactive thyrotropin (TSH) by Rana esculenta pituitaries (pars distalis) in vitro. Preincubation of the pituitaries with 50 ng/ml (64 nM) thyroxine (T4) for 6 hr suppressed the TRH- and oCRH-induced (268 nM) secretion of bioactive TSH, but did not affect the response of the pituitaries to 268 nM mGnRH. Triiodothyronine (T3) (64 nM) reduced both the TRH- and mGnRH-stimulated release of bioactive TSH; the response of TSH to TRH even decreased toward basal levels while a significant TSH response to mGnRH remained. In a separate experiment, pituitaries were preincubated for 6 hr with different equimolar doses of T3 and T4 (6.4, 32, and 64 nM); neither treatment affected the mGnRH-stimulated secretion of bioactive TSH. On the other hand, T4 suppressed the TSH response to TRH in a dose-dependent manner. The inhibitory effects of thyroid hormones on the TRH-induced release of bioactive TSH was present for at least 4 hr after their removal from the incubation medium. These results suggest that thyroid hormones exert a negative feedback control on the secretion of bioactive TSH in adult frogs by a direct action on the pars distalis. There may also be differences in thyroid hormone sensitivities of the TSH responses to mGnRH and TRH.
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PMID:Thyroid hormone feedback regulation of the secretion of bioactive thyrotropin in the frog. 149 May 87

Changes in the level of antidiuretic hormone (ADH), adrenocorticotropic hormone (ACTH), somatotropic hormone (STH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), prolactin (PL), thyroxin (T4), triiodothyronine (T3) and thyroxine-binding globulin (TBG) have been assessed before and during multiorgan excision in 22 donors with brain death. A progressing decrease in ADH blood supply and changes in ACTH, STH, FSH and PL content have been recorded. No regularities have been observed in LH level changes. TSH and thyroid hormone changes were in most cases characterized by a gradual decrease in their plasma levels. A drop in T3 concentration observed at the initial stage of the study was most pronounced with practically normal T4 and TBG values, that also decreased by the moment of heart excision. It has been concluded that brain death is accompanied by a considerable neuroendocrine disfunction and a marked syndrome of low T3 content.
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PMID:[Neuroendocrine disorders in brain-dead donors at the time of multiorgan harvesting]. 152 55

The sexually differentiated microsomal enzyme steroid 5 alpha-reductase (NADPH: delta 4-3-oxosteroid 5 alpha-oxido-reductase, EC 1.3.99.5) catalyzes the NADPH-dependent conversion of testosterone to 5 alpha-dihydrotestosterone, a more potent androgen. In rat liver, this enzyme is expressed at a 10-fold higher level in adult females as compared to adult males. The pituitary regulation of this enzyme and its mRNA was studied in untreated and hypophysectomized rats and in rats rendered hypothyroid by treatment with the antithyroid drug methimazole. Hepatic 5 alpha-reductase activity was elevated 8-fold, to 85% of adult female levels, in adult male rats given growth hormone by continuous infusion. This same treatment was only partially effective in restoring 5 alpha-reductase in rats depleted of endogenous growth hormone by hypophysectomy, indicating that other pituitary-dependent factors contribute to the elevation observed in the inact animals. Further analysis revealed that thyroxine, but not adrenocorticotropic hormone (ACTH) or chorionic gonadotropin, could elevate 5 alpha-reductase activity and mRNA when given to the hypophysectomized rats and that this effect was enhanced by the presence of growth hormone. This thyroid hormone dependence was confirmed by the decrease in hepatic 5 alpha-reductase expression in hypothyroid rats and by its substantial restoration following thyroxine replacement. Thyroxine also stimulated expression of another female-predominant hepatic mRNA, encoding the steroid 16 alpha-hydroxylase cytochrome P-450f (IIC7), in a manner that was independent of the stimulatory effect of growth hormone on this transcript. In contrast, thyroid hormone did not significantly affect protein or mRNA levels of the growth hormone-stimulated, female-specific steroid sulfate 15 beta-hydroxylase P-450 2d (IIC12). These findings establish that thyroid hormones act at a pretranslational level to modulate the expression of some, but not all, growth hormone-stimulated hepatic mRNAs and demonstrate that both thyroxine and growth hormone can independently contribute to the sex-dependent expression of hepatic enzymes of steroid metabolism.
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PMID:Pretranslational control by thyroid hormone of rat liver steroid 5 alpha-reductase and comparison to the thyroid dependence of two growth hormone-regulated CYP2C mRNAs. 217 47

To establish whether thyroid hormone modifies the heart rate directly or through an action on other neuroendocrine modulators, the authors have examined several animals models differing in the plasma levels of such compounds. Induction of the hypothyroid state in rats produced a slow onset of bradycardia, which may be removed by a prolonged triiodothyronine treatment. The involvement of TSH was excluded as, by comparing thyroidectomized, hypophysectomized and cold exposed rats, the heart rate was found to vary according to the thyroid levels and not to the TSH levels. Moreover growth hormone, corticotropin and gonadotropins do not influence the heart rate, as the bradycardia induced by hypophysectomy was fully removed by triiodothyronine treatment. The lack of influence by ACTH and GnH was confirmed by treatment of thyroidectomized rats with corticosteroids or testosterone, respectively. Finally, thyroid hormone did not act on the heart rate by changing the norepinephrine output at the sympathetic nerve endings in the heart. In fact, thyroidectomy produced a more intense bradycardia than sympathectomy, and such bradycardia was equally removed by triiodothyronine treatment in thyroidectomized rats and in thyroidectomized and then sympathectomized ones. The authors suggest that the direct effect of the thyroid hormone on cardiac chronotropism is due to an early enhancement of beta-adrenoceptors, followed by a late modification of the electrophysiological properties of the myocardium.
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PMID:The direct effect of the thyroid hormone on cardiac chronotropism. 248 2

The first case of isolated thyrotropin (TSH) deficiency with Cushing's syndrome was reported. A 46-year-old female was admitted to our hospital because of fatigability, puffy eye-lids, leg edema and petechia. She was treated with thyroid hormone. A low free triiodothyronine continued. Serum TSH was undetectable and serum thyrotropin releasing hormone (TRH) was elevated. No response of serum TSH and normal response of serum prolactin after administration of exogenous TRH suggested the abnormalities of anterior pituitary gland. The secretion of growth hormone and gonadotropin were intact, but the secretion of adrenocorticotropic hormone (ACTH) was impaired. A high level of serum cortisol, no response of serum ACTH by metyrapone test and a tumor mass of abdomen detected by computed tomography led to the diagnosis of Cushing's syndrome. Histological examination of the tumor revealed adrenal adenoma. Twenty two months after the surgery, serum ACTH level was normalized, but the secretion of serum TSH to exogenous TRH was still absent. The results indicated that hypothyroidism in our patient was due to isolated TSH deficiency.
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PMID:A case of isolated thyrotropin deficiency with Cushing's syndrome. 263 42

Circulating levels of corticotropin, thyroid hormones and insulin were measured in rats at various times after turpentine-induced inflammation. Corticotropin increased rapidly showing a biphasic response with a four-fold increase at about 6-8 hr after inflammation and a 10-fold increase at 10 hr after inflammation. The response of insulin to inflammation was slower than corticotropin and the magnitude of the increase was smaller. Insulin increased by three-fold at 20 hr after inflammation. Thyroid hormone levels were depressed by turpentine inflammation. Levels fell after 4 hr and remained at low levels throughout. Administration of a cytokine preparation to rats also caused depressed thyroxine levels at short intervals after administration. However, levels increased at longer intervals after administration. This suggests that, like corticotropin and insulin, thyroid hormone levels could be under the control of immunotransmitters during the acute phase response.
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PMID:Rat corticotropin, insulin and thyroid hormone levels during the acute phase response to inflammation. 288 47


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