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)

The effects of four day periods of infusions of 600 gm/24 hours glucose and 600 gm/24 hours of a combination of glucose, fructose, and xylitol were compared. This study was performed during total parenteral nutrition of twelve postoperative patients with major complications. The mean plasma glucose level was significantly lower during the infusion of the combination of sugars (154.2+/-19.5 mg/100 ml versus 193.9+/-15.0 mg/100 ml[p is less than 0.005). Furthermore, the required dosage of exogenous insulin was significantly lower (18.9+/-12.3 units/day versus 43.7+/-19.7 units/day [p is less than 0.01). Mean renal carbohydrate losses were 0.85 per cent during glucose infusion and 1.7 per cent during infusion of the combination. The influence of both infusion regimes on values for pH, base excess, lactate, pyruvate, free fatty acids, insulin, sodium, potassium, chloride, magnesium, phosphorus, bilirubin, alkaline phosphatase, SGOT, and SGPT 0.85 has been investigated. No clinical side effects were observed. It is concluded that the administration of the investigated combination of glucose, fructose, and xylitol is justified in patients in whom hyperglycemia during infusion of glucose alone is difficult to control with insulin.
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PMID:Comparison between glucose and a combination of glucose, fructose, and xylitol as carbohydrates for total parenteral nutrition of surgical intensive care patients. 40 88

Pharmacologic doses of triamcinolone hexacetonide were injected intramuscularly or intraarticularly in immature Papio papio baboons. The mandibular condyle served as a model for histologic examinations concerning the effect of glucocorticoid hormone on cartilage and bone. Biochemical examinations of blood and urine indicated the development of distinct hypophosphatemia, hypercalcemia followed by hyperphosphaturia, and hypocalciuria. Serum alkaline phosphatase activity rose during the initial phases of the experiment but decreased considerably after the sixth injection of the hormone. Hyperglycemia and an increase in serum amylase were noticed along with signs of moderate metabolic acidosis. Histologic examinations disclosed signs of severe destruction of cartilage and bone. By the sixth intraarticular injection, definite fibrillation was noted in the articular cartilage, followed by complete disappearance of cartilage. The subchondral bone appeared to be adversely affected by the hormone as it lost its typical lamellar organization and attained the characteristics of woven bone. The condyle showed clear signs of fibro-osseous transformation, with fibrosis as the dominant structural feature. The preceding biochemical and morphologic findings are indicative of parathyroid hyperactivity.
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PMID:Mechanisms involved in mandibular condylopathy secondary to intraarticular injections of glucocorticoids. 41 94

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

The rosy barb (Puntius conchonius) was exposed to copper (Cu) for short (48 hr) and long (8 weeks) terms and effects on enzyme activities and biochemical variables in the blood and tissues were examined. In vivo exposure to 571 micrograms CuSO4/liter (96-hr median tolerance limit (TLm)) for 48 hr stimulated to varying degrees acid phosphatase (AcP), alkaline phosphatase (AlP) (except in the liver), and acetylcholinesterase activities in selected tissues. The alanine aminotransferase and lactic dehydrogenase (LDH) (except in the heart) activities were inhibited to varying degrees in vivo. In vitro, the presence of 10(-6) M Cu suppressed enzyme activities in the tissues examined, with a few exceptions such as AcP in ovaries and gut, AlP in liver, gills, gut, and testes, and LDH in liver. Hyperglycemia, hyperlactemia, hyperproteinemia, elevated blood free fatty acid (FFA) levels, and hypocholesterolemia were manifested in the fish exposed to 190 micrograms CuSO4/liter (1/3 96-hr TLm). Effects on the tissues included glycogenolysis (liver and skeletal muscles), glycogenesis (brain and heart), a marked rise in hepatic proteins, accumulation of FFAs in liver and skeletal muscles, and reduction in hepatic and gonadal cholesterol contents. After 8 weeks, a trend toward recovery was noted in the biochemical variables (except blood and hepatic protein levels).
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PMID:Short- and long-term effects of copper on the rosy barb (Puntius conchonius Ham.). 137 34

Chemically induced diabetes has been reported to induce profound changes in bile formation, but possible toxic effects of the streptozotocin or alloxan used cannot be excluded totally. This study was undertaken to evaluate biliary function in spontaneously diabetic female biobreeding rats with a diabetes duration of 2 wk and compare them with nondiabetic littermates. Diabetic animals evidenced glycosuria, hyperglycemia and hypoinsulinemia. Biliary concentration and secretion of bile acids, cholesterol and phospholipids were significantly increased, with no enhancement in the lithogenic index of bile. Bile flow and the biliary secretion of sodium, potassium, chloride and bicarbonate were significantly reduced despite the increased bile acid secretion. The cholestatic condition was confirmed by an increased serum concentration of bile acids and a higher activity in serum of the alkaline phosphatase liver isoenzyme. Biliary calcium concentration increased without any change in its serum concentration. A linear relationship was observed between biliary calcium and bile acid secretion. Serum concentration of unconjugated and of conjugated bilirubin was increased 1.6-fold and 8-fold, respectively, with a 1.5-fold enhanced biliary secretion of bilirubins despite the cholestasis; this points to an enhanced bilirubin production. An increased proportion of conjugated bilirubin was found in serum together with an enhanced bilirubin diconjugate/monoconjugate ratio in bile. A higher UDP-glucuronyltransferase activity and a delayed transit of bilirubin could account for these effects. Administration of insulin to diabetic animals tended to reverse the above reported changes. The spontaneously diabetic biobreeding rat thus represents a model of bile acid-independent cholestasis with enhanced biliary bile acid and calcium secretion and with presumably an enhanced bilirubin production.
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PMID:Spontaneously diabetic biobreeding rats and impairment of bile acid-independent bile flow and increased biliary bilirubin, calcium and lipid secretion. 163 53

Changes in intestinal transport of L-amino acid and D-glucose in streptozotocin (STZ)-induced hyperglycemic guinea-pig were examined using brush-border membrane vesicles. The vesicles were prepared from guinea-pigs on days 3, 10, and 21 after intravenous injection of STZ (150 mg/kg body weight), and from control animals injected with sodium citrate buffer (pH 4.5) in the same manner. Blood glucose concentration rose to greater than 300 mg/dl in the hyperglycemic guinea-pigs 24 h after STZ injection, and then remained constant. All vesicles obtained under different conditions showed a similar specific activity of alkaline phosphatase, a marker enzyme of the intestinal brush-border membrane, indicating a similar purity of the membrane vesicles. On day 3, Na(+)-dependent amino acid transport was found to be approx. 30% higher in the hyperglycemic than in the control group, and Na(+)-dependent glucose transport was 35% lower in the hyperglycemic than in the control group. On days 10 and 21, Na(+)-dependent amino acid transport had recovered to the control levels, whereas Na(+)-dependent glucose transport was twice as high as in the hyperglycemic than in the control group. Na(+)-independent amino acid and Na(+)-independent glucose transport showed no difference between the hyperglycemic and control groups after STZ injection. The changes in both Na(+)-dependent amino acid and glucose transport were attributed to significant changes in the Vmax values with no change in the apparent Km values. This study clearly demonstrates that hyperglycemia is associated with reciprocal changes in intestinal transport of amino acid and glucose in its acute phase, suggesting an important pathophysiological regulatory mechanism for absorption of nutrients by control of the numbers of specific carriers.
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PMID:Changes in amino acid and glucose transport in brush-border membrane vesicles of hyperglycemic guinea-pig small intestine. 182 12

1. Two hours of exposure to heat stress, resulted in hyperthermia in rabbits (Oryctolagus cuniculus). 2. This was accompanied by a severe hypocapnia, partly compensated for by a significant decrease in bicarbonate (HCO3-) concentration. 3. The severest hyperthermia (Tb = 43.5 degrees) was followed by a sharp decreased in both PaCO2 (to 20.2 torr) and HCO3- (to 9.2 mM/l), resulting in extreme metabolic acidosis (pH = 7.290). 4. The significant increase in serum osmolality (27%) is interpreted by the cumulative effect of increased electrolyte and metabolite concentrations. 5. The elevation in blood BUN, creatinine, globulin and GOT levels point to a possible damage to muscle cells by hypothermia. 6. The stable cholesterol and alkaline phosphatase levels, suggest that liver tissue was not damaged. 7. The dramatic increase in glucose from 103.8 to 348.8 mg%, and the significant increase (from 22.0 to 39.9 mg%) in BUN, suggest a possible disability of the cells to metabolize carbohydrates, accompanied by a progressive proteolysis as an alternative process for energy production. 8. The data suggest that the emergence of muscle cell damage, severe hyperglycemia and acidosis under heat stress, precedes and amplifies the deteriorating effects of high Tb in heat stressed rabbits, which often lead to mortality.
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PMID:The effect of heat exposure on blood chemistry of the hyperthermic rabbit. 198 37

Transient hyperglycemia in patients receiving total parenteral nutrition may be associated with impaired immune function. The effects of short-term hyperglycemia on one aspect of antimicrobial immune function, ie, the ability of IgG to fix complement, were investigated. Aliquots of anti-human albumin, anti-horse ferritin, and anti-alkaline phosphatase were incubated for 0, 8, 16, 24, 48, and 96 hr with either 0 or 240 mg of glucose per deciliter of buffer. All samples were analyzed for the degree of glycation using a thiobarbituric acid assay, and for complement fixation ability using a microcomplement fixation assay. Significant increases in glycation over control samples were observed after only 16 hr (31 vs 15 mmol 5-hydroxymethylfurfural/mol IgG, p less than 0.01). Complement fixation was significantly altered after 48 hr of incubation (76 +/- 5% vs 90 +/- 8% total serum complement fixed by albumin/anti-albumin complex, p less than 0.03) when four of the 84 (4.7%) IgG lysine residues were glycated. It is demonstrated that a significant reduction in complement fixation by immunoglobulin occurs with elevated glucose concentrations and that this may play a clinically significant role in transiently hyperglycemic patients.
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PMID:Nonenzymatic glycosylation of immunoglobulin G impairs complement fixation. 200 35

Kinetic studies of the histochemical and histoenzymatic behavior of rabbit pancreatic parenchymas were performed 5, 30 and 90 days after Wirsung duct ligation. In control pancreas, some enzyme activities (EA) were more prominent in Langerhans islets [glucose-6-phosphatase, glucose-6-phosphate dehydrogenase (DH), isocitrate DH, glycerol-3-phosphate DH, NADPH DH], others were strongly marked in acini and ducts (alkaline phosphatase, beta-glucuronidase, acid esterase aryl-sulfatase). Histochemical and enzyme abnormalities observed in experimental rabbits reflect the post-ligation degenerative and reactive processes in both exocrine and endocrine pancreas: (1) the decrease in Krebs cycle and pentose pathway linked EA and the increased lysosomal and acid phosphatase EA reflect early (day 5) degeneration and necrosis of islets and acini (day 30); (2) proliferative processes in developed ductal epithelia are shown by an increase in both glycolytic and lysosomal EA (days 30 and 90); (3) connective tissue neogenesis and interstitial fibrosis occurred as shown by activated beta-glucuronidase, aryl-sulfatase, alkaline phosphatase and increased ribonucleoproteins and glycoaminoglycans contents (day 30); (4) on day 90, the neoformed cell clusters presenting glucose-6-phosphatase positivity (B-cell marker) are seen in the pancreas remnant. At the same time, blood insulin level increases correlated with a decrease of hyperglycemia.
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PMID:Cell features in pancreas of prediabetic and diabetic rabbits after Wirsung duct ligation. Histochemical and histoenzymatic studies. 233 24

Recent studies show that acute and chronic hyperglycemia cause a diffuse decrease in regional cerebral blood flow and that chronic hyperglycemia decreases the brain L-glucose space. Since these changes can be caused by a decreased density of perfused brain capillaries, we used 30 adult male Wistar rats to study the effect of acute and chronic hyperglycemia on 1) the brain intravascular space using radioiodinated albumin, 2) the anatomic density of brain capillaries using alkaline phosphatase histochemistry, and 3) the fraction of brain capillaries that are perfused using the fluorescein isothiocyanate-dextran method. Our results indicate that acute and chronic hyperglycemia do not affect the brain intravascular space nor the anatomic density of brain capillaries. Also, there were no differences in capillary recruitment among normoglycemic, acutely hyperglycemic, and chronically hyperglycemic rats. These results suggest that the shrinkage of the brain L-glucose space in chronic hyperglycemia is more likely due to changes in the blood-brain barrier permeability to L-glucose.
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PMID:Brain perfusion in acute and chronic hyperglycemia in rats. 266 99


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