Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Because of the organ and enzyme specificity of the metabolism of galactose, evaluation of various kinds of liver disease can be done by measuring the formation of labeled breath CO2 from carbon-labeled galactose in vivo. As shown earlier with uniformly 14C- or 13C-labeled galactose, a further study of alcoholic cirrhotic patients and controls with cheaper 1-14C-galactose indicates a superior discriminatory value of this test compared with common liver function tests. The oxidation test is easier to perform and more acceptable to patients than the standard galactose tolerance blood test. Output of 14CO2 showed slight correlations with serum albumin and 99mTc-sulfur colloid scan grade, but not with other function tests (SGOT, alkaline phosphatase, bilirubin). Comparison with five-year clinical outcome (two groups: with or without known liver-related death) in 29 of 43 total cirrhotic patients (U-14C or 1-14C-galactose) showed a low (75% probability) significance of prognosis for the galactose oxidation test, but none for any of the other tests. A two-part test of oxidation of 14C-galactose (with and without an acute dose of ethanol) in 19 possibly or likely alcoholic (but non-cirrhotic) persons indicated, by correlation with other liver function tests and drinking history, some possibly enhanced sensitivity of the two-part versus the single test for recognizing early liver damage. A preliminary study of the single galactose oxidation test in 7 patients with Type II diabetes suggests moderate impairment of oxidation, which might be applied to evaluate the hepatic disorder in diabetes.
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PMID:Impaired oxidation of carbon-labeled galactose by alcoholic or diabetic liver in vivo. 367 Oct 97

Dexamethasone is an important regulator of cellular proliferation and differentiation, but paradoxical effects have been noted in a variety of culture systems. The purpose of this study was to determine whether dexamethasone induces proliferation and differentiation of osteogenic precursor cells. Periosteal explants from embryonic chicks were grown in culture for 3 or 4 days, treated continuously with dexamethasone or ethanol vehicle, and then either pulse-labeled with 3H-thymidine at 3 days or labeled for 24 hr between day 3 and day 4. Histochemical and autoradiographic procedures were used to assess the proliferation and differentiation of osteogenic cells. At 3 days, the area of bone, the percentage of alkaline phosphatase-positive cells, the percentage of 3H-thymidine-labeled cells, and the percentage of cells labeled with both markers were significantly higher in dexamethasone-treated cultures. Between day 3 and day 4 no significant changes in these parameters were observed in the dexamethasone-treated cultures. In comparison, control cultures exhibited significant increases in the percentage of 3H-thymidine-labeled cells after 24 hr of continuous labeling. The data show that dexamethasone induces a burst of proliferation in a cohort of cells that undergo differentiation. Once these cells have divided, further proliferation within the culture is limited. Finally, it is apparent that the timing of experiments may be critical in determining whether dexamethasone will inhibit or stimulate proliferation.
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PMID:Dexamethasone induces proliferation and terminal differentiation of osteogenic cells in tissue culture. 374 Apr 74

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending on whether glycogen stores are adequate, inhibits protein synthesis, and results in fatty liver and in elevations in serum triglyceride levels. Increases in high-density lipoprotein cholesterol after ethanol ingestion may explain the lower risk of myocardial infarction and death from coronary disease after moderate drinking. Increases in serum lactate, resulting from the increased NADH/NAD+ ratio, and hyperuricemia, most likely the result of increased turnover of adenine nucleotides, are common transient effects of ethanol ingestion. Causes of vitamin deficiencies in alcoholism are decreased dietary intake, decreased intestinal absorption, and alterations in vitamin metabolism. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Ethanol decreases hepatic vitamin A concentration and its conversion to active retinal, and modifies renal metabolism of vitamin D.
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PMID:Metabolic effects of alcohol. 388 Dec 85

Cultured heart muscle cells, but not HeLa cells, oxidize long-chain fatty acids in medium containing dialyzed serum. Addition of chicken serum dialysate (or non-dialized serum) stimulated palmitic acid oxidation by HeLa cells 10 to 20 fold. This serum activity was not eliminated by lipid extraction, ethanol or acid precipitation, alkaline phosphatase treatment, or autoclaving. About 80% was lost after any one of the following treatments: 6N HCl at 110 degrees C for 16 hr, pepsin, Dowex cation exchange at pH 3, or 1N KOH at 100 degrees C for 1 hr. Serum activity was separated into five or more peaks by gel filtration with Sephadex G-10. Each of these peak fractions was further purified by HPLC using a cyanopropyl-bonded resin. Carnitine, which is important for the transport of long-chain fatty acids into mitochondria for oxidation, also stimulated the oxidation of palmitate. However, these serum factors are not known precursors to carnitine since its immediate precursor 4-n-trimethylaminobutyrate, did not stimulate palmitate oxidation. Total carnitine, including that in acylcarnitine compounds, was approximately 15 microM in the chicken sera to give approximately 0.7 microM in the medium. Based on the fraction of total activity accountable by carnitine and fractional stability to acid, alkali, and pepsin, about 75% of the activity is from non-carnitine compounds. Only one of the factors appears to be carnitine or an acylcarnitine derivative. Several lines of evidence suggest that the other factors are peptide compounds.
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PMID:Serum factors that stimulate fatty acid oxidation: properties of factors. 394 93

Two groups of rats were pair-fed diets in which 36% of the calories were provided by either ethanol or dextrimaltose. After 60 days on these liquid diets, rats fed ethanol were significantly smaller than control rats fed dextrimaltose. Serum cholesterol levels in ethanol-fed animals were 20% higher than control rats. Cholestasis was not observed histologically, and serum alkaline phosphatase and bilirubin levels were the same in both groups. The livers of animals ingesting ethanol accumulated triglycerides and cholesterol. The increase in cholesterol was due to an increase in cholesteryl esters. The cholesterol content of liver microsomes, however, was unchanged by ethanol feeding. A small increase in unesterified cholesterol was observed in intestinal microsomes prepared from animals receiving ethanol. Microsomal fatty acids in liver and intestine were unchanged by the ethanol diet. Chronic ingestion of ethanol in these animals failed to change acyl coenzyme A:cholesterol acyltransferase or 3-hydroxy-3-methylglutaryl-coenzyme A reductase activities in the intestine. In contrast, the activities of acyl coenzyme A:cholesterol acyltransferase and 3-hydroxy-3-methylglutaryl-coenzyme A reductase were significantly increased in the livers of rats receiving ethanol. Thus, the chronic ingestion of ethanol caused a marked accumulation of hepatic cholesteryl esters. This was associated with a significant increase in the activities of enzymes that control the rates of both cholesterol synthesis and cholesterol esterification in the liver. These observed changes in enzyme activities may contribute to the lipid accumulation which occurs in these livers. Chronic ethanol consumption did not alter cholesterol metabolism in the intestine.
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PMID:Effect of chronic ethanol ingestion on hepatic and intestinal acyl coenzyme a:cholesterol acyltransferase and 3-hydroxy-3-methylglutaryl coenzyme a reductase in the rat. 396 54

In 12 uraemic patients with symptomatic secondary hyperparathyroidism, 13 parathyroid hyperplasias, detected by sonography and confirmed by fine-needle aspiration biopsy, were treated by ultrasonically-guided percutaneous injection of absolute ethanol, in order to reduce the gland mass. Only in the larger glands were significant volume reductions recorded, whereas in the smaller ones evident structural changes were observed. In most cases with single lesions, a reduced incidence of vitamin D hypercalcaemia and a permanent improvement in bone alkaline phosphatase and PTH were documented. This technique can be usefully employed either as an alternative to surgery in selected cases, or as support to medical therapy in single lesions.
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PMID:Ultrasonically guided fine-needle alcohol injection as an adjunct to medical treatment in secondary hyperparathyroidism. 399 88

The aim of this study was to investigate possible mechanisms involved in the elevation of serum alkaline phosphatase activity in alcoholics. Male Sprague-Dawley rats were pair-fed nutritionally adequate liquid diets containing ethanol as 36% of energy or an isocaloric amount of carbohydrate for 4-5 wk. Serum alkaline phosphatase activity was increased moderately but significantly. Hepatocytes isolated from ethanol-fed animals exhibited pronounced morphologic alterations of their plasma membranes by scanning electron microscopy and a reduced content of alkaline phosphatase despite an increase in total liver alkaline phosphatase content. Chronic ethanol feeding also potentiated the release of alkaline phosphatase from the cells during incubation with 50 mM ethanol. Furthermore, chronic ethanol feeding resulted in reduced recovery of alkaline phosphatase in hepatic plasma membranes isolated by sucrose gradient centrifugation but did not affect the recoveries of other plasma membrane markers (5'-nucleotidase and Na+,K+-adenosine triphosphatase) nor the subcellular distribution of alkaline phosphatase in the nuclear, mitochondrial, microsomal, and cytosolic fractions. These findings suggest that the increased serum alkaline phosphatase levels observed in response to chronic ethanol feeding may be due, at least in part, to increased lability of this plasma membrane enzyme.
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PMID:Chronic ethanol consumption alters rat liver plasma membranes and potentiates release of alkaline phosphatase. 403 95

Using the interferometric technique the authors studied the effect of simultaneous administration of ibuprofen (Polfa) and ethanol on the activity of alkaline phosphatase in the proximal jejunum. Both ibuprofen and ethanol cause in the digestive tract functional and morphological changes. The used technique of quantitative determination of alkaline phosphatase activity at the site of its primary location made possible an assessment of changes in the activity of the enzyme caused by the administered agents. It was found that after 60 days of the experiment both agents caused a statistically greater changes were observed in the rats receiving both these agents simultaneously. The obtained results suggest the conclusion that simultaneous administration of ibuprofen and ethanol causes in the mucosal gland in the proximal small intestine development of an interaction of the additive.
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PMID:Effect of simultaneous administration of ibuprofen and ethanol on the alkaline phosphatase activity in the small intestine. 404 39

31 healthy Thai males, 22 Thai male regular drinkers not suffering from any clinical signs or symptoms of alcoholism, and 52 patients from a neurological hospital in Bangkok suffering from the effects of chronic alcohol consumption were investigated. Alcohol consumption in asymptomatic drinkers ranged from 7 to 134 (median 44) g/d ethanol, and for the patients 22 to 517 (median 197) g/d ethanol, as assessed by questionnaires. The symptomatic alcohol drinkers had consumed alcohol for 2 to 35 years and the hospitalized patients for 5 to 40 years. Only the median levels of serum triglycerides and serum glutamyl transferase (gamma-G) were significantly increased and vitamin B1 deficiency was found with higher frequency in the group of alcohol drinkers without clinical signs compared with the healthy non-alcohol drinkers. Statistically significant correlations were demonstrated in the group of asymptomatic alcohol drinkers only, between alcohol consumption and the Quetelet's index, gamma-G, and alkaline phosphatase levels. Alkaline phosphatase also correlated significantly with gamma-G. In the group of hospitalized patients, compared with healthy males statistically significantly higher median values of systolic and diastolic blood pressure, serum triglyceride, gamma-G, aspartate aminotransferase (GOT), alanine aminotransferase (GPT), alkaline phosphatase, haemoglobin, hematocrit, folate and total protein were found. The median levels of cholesterol, bilirubin, vitamin B2, B6 and B12 in the hospitalized group were lower than, but not significantly different from the other two groups.
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PMID:Alcohol consumption, liver function tests and nutritional status in Thai males. 612 Jan 45

To study the effect of chronic alcohol administration on the activities of liver plasma membrane enzymes such as gamma-glutamyltransferase, alkaline phosphatase and 5'-nucleotidase, female rats were pair-fed for 6 weeks nutritionally adequate liquid diets containing either ethanol or isocaloric carbohydrates as controls. Compared to the control diet, chronic alcohol administration resulted in a significant enhancement of serum activities of gamma-glutamyltransferase, alkaline phosphatase and 5'-nucleotidase by 91% (P less than 0.005), 80% (P less than 0.001) and 65% (P less than 0.01), respectively. Concomitantly, chronic alcohol intake led to a striking increase of gamma-glutamyltransferase activities in liver homogenates by 68% (P less than 0.001), in liver plasma membranes rich in bile canaliculi by 80% (P less than 0.025), and in liver plasma membranes free of bile canaliculi by 24% (P less than 0.02). However, chronic ethanol consumption had no effect on alkaline phosphatase activities in liver homogenates and liver plasma membranes but significantly suppressed 5'-nucleotidase activities. These results therefore show that chronic intake of ethanol increases serum activities of enzymes originating from liver plasma membranes but has different effects on the enzyme activity in liver plasma membranes itself, suggesting that the alcohol-mediated increase of serum activities of various enzymes originating from liver plasma membranes might be due to different mechanisms.
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PMID:Effect of chronic alcohol consumption on the activities of liver plasma membrane enzymes: gamma-glutamyltransferase, alkaline phosphatase and 5'-nucleotidase. 612 53


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