Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HgC12-induced renal tubular lesions in the rat present histochemically with a transitory decrease of alkaline phosphatase, adenosinetriphosphatase (ATPase), and leucine-aminopeptidase activity. The toxic alterations of enzyme activity were more pronounced in the pars recta of the proximal tubule and in the loop of Henle, as compared with the tubulus contortus I. L-thyroxine treatment leads to an accelerated reversal of that enzymatic defect, followinga characteristic pattern, and to a differentiating increase of acid phosphatase and ATPase activity in certain parts of the normal renal tubule. The observations are discussed with reference to the specific mode of action of sublimate and l-thyroxine upon the tubular enzymes and to the well-known metabolic and functional influences of thyroid hormone on the kidney.
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PMID:Influence of L-thyroxine upon enzymatic activity in the renal tubular epithelium of the rat under normal conditions and in mercury-induced lesions. I. Histochemical studies of alkaline phosphatase, acid phosphatase, adenosine- tri-phosphatase and leucine-aminopeptidase. 19 Jul 63

A thyroid hormone analogue, sodium dextro-triiodothyronine (NaDT3), at a dosage of 1 mg/day for 1 or 2 yr, decreased serum cholesterol levels about 30% in 26 hyperlipidemic adults. There were less sustained decreases in the serum phospholipids, and occasional lowering of the serum triglycerides, but no effects on body weight, blood pressure, or pulse rate. Changes recognized as variable concomitants of spontaneous or induced thyrotoxicosis, such as transient increases in fasting blood glucose, calcium, and globulin, persistent rises in alkaline phosphatase, and nonsustained decreases in hematocrit are consonant with the fact that Na-DT3 exerts about one tenth of the thyroid hormone activity of LT3. These changes, however, appear to represent actions of iodinated amino acids apart from those effects that result in clinical thyrotoxicosis.
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PMID:Thyroid hormone-like effects without thyrotoxicosis during one year's therapy with NA-DT3 for hypercholesterolemia. 77 45

1. Standard laboratory values of blood samples taken from Weddell seals in Antarctica were determined. 2. Numerous blood parameters are similar to those observed in man. 3. Comparatively high cholesterol levels but normal triglyceride levels were observed when compared with humans. 4. In comparison to laboratory findings in humans, T4 levels were decreased although T3 levels were normal. 5. The levels of alkaline phosphatase are considerably higher than those in humans. 6. The data obtained indicate different lipid and thyroid hormone metabolism in Weddell seals when compared with humans.
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PMID:Basic biochemical data on blood from antarctic Weddell seals (Leptonychotes weddelli): ions, lipids, enzymes, serum proteins and thyroid hormones. 135 37

The historical and clinical features and the haematological and biochemical changes in 126 cats with hyperthyroidism are described; 125 of the cats were domestic short- or longhaired, and one was a chinchilla. There were 62 males and 64 females with a mean age of 13.0 years. The duration of signs ranged from two days to two years with a mean of 5.4 months. The historical and clinical features were weight loss, polyphagia, polyuria/polydipsia, tachycardia, hyperactivity, diarrhoea, respiratory abnormalities, other cardiac abnormalities, skin lesions, vomiting, moderately raised temperature, decreased activity, decreased appetite, congestive cardiac failure, haematuria and intermittently decreased appetite. Goitre was palpable in 123 cats. The serum total thyroxine concentrations of the cats were more than three standard deviations above the mean of the reference range. Serum total tri-iodothyronine concentrations ranged from 0.78 to 14.96 nmol/litre and were within the reference range in 11 of the cats. Mild hyperthyroidism was a much commoner cause of high normal or marginally above normal thyroid hormone concentrations than severe, concurrent, non-thyroidal illness. Other common biochemical changes were increased of serum alanine aminotransferase, urea, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase. There were minimal changes in the red cell parameters. Leucocyte changes showed two trends: a mature neutrophilia, either with or without an accompanying leucocytosis often in association with a lymphopenia, or an eosinophilia, either with or without a lymphocytosis.
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PMID:Historical, clinical and laboratory features of 126 hyperthyroid cats. 141 11

Patients taking suppressive doses of thyroid hormones may have adverse effects from such treatment. To test conditions under which such treatment might be deleterious to bone, we studied a group of patients who had undergone thyroidectomy because of thyroid cancer 1 to 21 years previously and were treated with steady suppressive doses of exogenous thyroid hormone. The group consisted from 13 men, 20 premenopausal and 25 postmenopausal women. The level of serum tyroxin a trijodothyronin in average didn't differ from the control subjects; thyreostimulating hormone was significantly lower than in controls. Vertebral bone density (BMD) was significantly reduced and biochemical markers of bone formation and (osteocalcin and bone isoenzyme of alkaline phosphatase in serum) were significantly increased as compared with controls only in postmenopausal patients. Biochemical indices of bone resorption (urinary hydroxyproline and plasma tartrate resistant acid phosphatase activity) were significantly increased in premenopausal and also in postmenopausal women. In thyroid hormone treated women, biochemical indices of both bone resorption and bone formation correlated significantly negatively with serum TSH levels. The results suggest that in postmenopausal women there is no "safe" suppressive dose of thyroid hormone. Patients treated with thyroid hormone should be evaluated for a latent or early symptomatic stage of bone loss. The thyroid drugs used should consist of exact content of thyroid hormones, preferably thyroxin.
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PMID:[The risk for osteoporosis in persons treated with thyroid hormones]. 148 84

Assays were developed to detect and measure autoantibodies (AA) to thyroglobulin (Tg) and to the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). An ELISA to detect AA to Tg was developed, using purified canine Tg as the antigen and goat anti-canine IgG conjugated with alkaline phosphatase as the second antibody. A highly charged agarose electrophoresis assay was used for determination of AA to T4 and T3. Sera from dogs (n = 119) with clinical signs consistent with hypothyroidism were tested for AA to Tg, T4, and T3. Autoantibodies to at least 1 of the 3 thyroid antigens were detected in 58 of the 119 (48.7%) sera tested. Autoantibodies to Tg were detected more frequently in samples with low serum concentrations of thyroid hormones than in samples with normal concentrations. The presence of AA to T4, T3, or both was not significantly associated with low thyroid hormone concentrations, but this lack of association may have been attributable to binding of AA in the measurement of thyroid hormones by radioimmunoassay.
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PMID:Prevalence of autoantibodies to thyroglobulin, thyroxine, or triiodothyronine and relationship of autoantibodies and serum concentrations of iodothyronines in dogs. 158 11

To test conditions under which thyroid hormone might be deleterious to bone, we studied a group of 58 patients who had undergone thyroidectomy because of thyroid cancer 1 to 21 years previously and were treated with steady doses of exogenous thyroid hormone. Vertebral bone density (BMD Z-score) was significantly reduced and biochemical indices of bone resorption (urinary hydroxyproline and plasma tartrate-resistant acid phosphatase activity) and of osteoblastic activity (plasma osteocalcin and bone isoenzyme of serum alkaline phosphatase) as well as the calculated prevalence of bone resorption relative to osteoblastic activity (HBP) were significantly increased in thyroid hormone-treated post-menopausal women but not in men and premenopausal women. The HBP as well as the biochemical indices of bone remodeling were significantly negatively correlated with serum TSH levels. In treated patients, BMD Z-score was significantly dependent on the HBP, menopausal state, duration of treatment and serum TSH levels. In conclusion, the further increase in bone resorption by thyroid hormone is predisposed by menopausal changes in bone turnover. The simultaneous evaluation of biochemical indices of bone resorption and formation improves the assessment of bone loss in patients treated with thyroid hormone in a suppressive dose.
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PMID:Biochemical assessment of bone loss in patients on long-term thyroid hormone treatment. 162 31

We have previously shown that osteocalcin synthesis is readily induced by 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in MG-63 human osteosarcoma cells (Mahonen et al. (1990) Biochim. Biophys. Acta 1048, 30-37). In the present study, the regulation of osteocalcin synthesis by other hormones of the steroid-thyroid hormone family (retinoic acid, 17 beta-estradiol, triiodothyronine, and dexamethasone) was examined. We found that the other hormones alone had no effects on medium osteocalcin and osteocalcin mRNA concentrations by 96 h of treatment. Compared with 1,25(OH)2D3, however, the combination of 1,25(OH)2D3 with dexamethasone resulted in a greatly reduced medium osteocalcin concentration. Also estradiol and triiodothyronine diminished the stimulatory effect of 1,25(OH)2D3. In contrast, the combination of 1,25(OH)2D3 with retinoic acid resulted in an increased medium osteocalcin concentration. The inhibition of osteocalcin synthesis by dexamethasone and triiodothyronine was accompanied by decreased osteocalcin mRNA levels. Retinoic acid and estradiol, however, did not influence the 1,25(OH)2D3-induced osteocalcin mRNA levels. To examine the specificity of the hormonal effects, the activity of alkaline phosphatase was determined. Both baseline and 1,25(OH)2D3-stimulated alkaline phosphatase activity was found to be inhibited by all other hormones. These results suggest that the steroidal hormones specifically affect osteocalcin synthesis in osteoblastic bone cells, and that complex interactions occur at the level of transcription and/or translation resulting in each case in a finely adjusted rate of osteocalcin synthesis.
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PMID:Modulation of 1,25(OH)2D3-induced osteocalcin synthesis in human osteosarcoma cells by other steroidal hormones. 182 Sep 70

In a retrospective study of liver function tests in subacute thyroiditis, 13 out of 22 patients with the disease demonstrated an elevation of alkaline phosphatase level. Less prevalent abnormalities were elevations in gamma-glutamyl transpeptidase (5 pts), alanine (4 pts) and aspartate (3 pts) aminotransferase activities. These enzyme alterations were not correlated with thyroid hormone levels, concomitant diseases, drugs or alcoholic intake, and normalized in six patients followed until recovery. A benign, short-lived and subclinical hepatic involvement is common in subacute thyroiditis.
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PMID:Liver enzyme abnormalities in subacute thyroiditis. 198 Oct 99

Because of the bone remodelling it induces, hyperthyroidism modifies the parameters of calcium-phosphorus metabolism. For a better determination of the mechanism involved, we studied 13 patients with Graves' disease compared with 13 controls. We measured the various parameters of calcium-phosphorus metabolism, notably the levels of parathormone, 25-hydroxycholecalciferol, 1-25 dihydroxycholecalciferol and ostocalcin; 8 patients were re-examined in euthyroidism. Total and corrected values of calcaemia (P less than 0.05 and P less than 0.01), phosphoreamie (P less than 0.01), alkaline phosphatase (P less than 0.01), calciuria (P less than 0.01) and hydroxyprolinuria (P less than 0.01) were significantly higher in patients with hyperthyroidism. Osteocalcin also was significantly increased (P less than 0.01) and correlated with thyroid hormone levels, thus confirming its usefulness as marker of bone remodelling in hyperthyroidism. Creatininaemia was significantly lowered (P less than 0.01). The intestinal absorption of calcium after injection of 1 g of calcium was reduced. Parathormone and 25-hydroxycholecalciferol levels were not significantly different in patients and in controls. In patients who were re-examined in euthyroidism, there was a significant increase in parathormone and in 1-25 dihydroxycholecalciferol levels (P less than 0.05). Thus, in situations of hyperthyroidism 2 elements contribute to a deficit in calcium balance: (a) a fall in parathormone level, consecutive to a rise in calcaemia, induces hypercalciuria; and (b) a fall in 1-25 dihydroxycholecalciferol level, consecutive to functional hypoparathyroidism and hyperphosphoraemia, results in a decrease of intestinal calcium absorption.
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PMID:[Phosphorus-calcium metabolism in hyperthyroidism]. 213 61


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