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In liver

Vitamin B,2 is produced by the growth of certain micro-organisms, and occurs also in liver, being the extrinsic anti-pernicious anaemia factor the isolation of which was sought for many years. [Pg.423]

Sotalol is rapidly and almost completely (>90%) absorbed. Bioavahabhity of absorbed dmg is 89—100%. Peak plasma levels are achieved in 2—4 h. Sotalol is 50% bound to plasma proteins. Plasma half-life of the compound is about 5.2 h. No metabolites of sotalol have been identified indicating littie metabolism. The dmg is excreted mainly by the kidneys (80—90%) and about 10% is eliminated in the feces. The plasma half-life is prolonged in patients having renal failure. Kinetics of the compound are not affected by changes in liver function (1,2). Sotalol has ah the adverse effects of -adrenoceptor blockers including myocardial depression, bradycardia, transient hypotension, and proarrhythmic effects (1,2). [Pg.121]

Oxyphenbutazone (712), y-hydroxyphenylbutazone and kebuzone (715) are metabolites of phenylbutazone in liver. The first cited is an equally potent antiinflammatory agent but slightly less toxic. Compounds (711) and (712) are rarely used as analgesics and antipyretics because of their toxicities. The first one is used in therapy of rheumatoid disorders characterized by a lack of detectable antiglobulin and antinuclear antibodies in the serum. The y-hydroxyphenylbutazone has marked uricosuric activity but little antirheumatic effect. Kebuzone (715) is an antiinflammatory agent still widely used in Europe. [Pg.296]

The specimens analyzed are the punctures of human liver. This provides the life-time investigation of elemental metabolism in liver of patient. This is very important aspect, because the information obtained from autopsy is distorted because of fast processes in the liver post mortem. [Pg.387]

Insulin is a peptide hormone, secreted by the pancreas, that regulates glucose metabolism in the body. Insufficient production of insulin or failure of insulin to stimulate target sites in liver, muscle, and adipose tissue leads to the serious metabolic disorder known as diabetes mellitus. Diabetes afflicts millions of people worldwide. Diabetic individuals typically exhibit high levels of glucose in the blood, but insulin injection therapy allows diabetic individuals to maintain normal levels of blood glucose. [Pg.207]

FIGURE 24.28 The formation of ketone bodies, synthesized primarily in liver mitochondria. [Pg.799]

Even though acetate units, such as those obtained from fatty acid oxidation, cannot be used for net synthesis of carbohydrate in animals, labeled carbon from " C-labeled acetate can be found in newly synthesized glucose (for example, in liver glycogen) in animal tracer studies. Explain how this can be. Which carbons of glucose would you expect to be the first to be labeled by "Relabeled acetate ... [Pg.800]

AlOiOHl bep 0 lOHl wiib chains of oclahedra sl-a ked in livers inlerconneUed wiib H bonds. sid Al in cerkiii ockibcdral sites... [Pg.243]

Inoue, S., et al. (1983). Trace characterization of the Watasenia luciferin in eye and skin photophores and in liver of Watasenia scintillans. Agric. Biol. Chem. 47 635-636. [Pg.406]

There is weak expression of PPARy in muscle, liver and other tissues, enabling TZDs to support the effects of insulin in these tissues, notably increased glucose uptake in muscle and reduced glucose production in liver. TZDs may also affect nutrient metabolism by skeletal muscle through a direct mitochondrial action that is independent of PPARy. [Pg.120]

Tissue expression Mainly white and brown adipose tissue weak expression in liver, muscle, gut, macrophages, pancreatic (3-cells and haemopoietic tissues... [Pg.121]

Hofmann AF (1999) The continuing importance of bile acids in liver and intestinal disease. Arch Intern Med 159 2647-2658... [Pg.259]

Primarily hydrolyses esters with longer aliphatic (compared to AChE) or aromatic acyl moiety, such as butyrylcholine (BCh) and benzoylcholine (BzCh). BChE is the primary circulating ChE. It is threefold more abundant than AChE in human blood and is found in liver, lungs, muscles, brain and heart. [Pg.357]

The main mineralocorticoid agonist in humans is aldosterone. Additionally, cortisol, corticosterone, and DOC have also mineralocorticoid agonistic activity. The synthetic steroid fludrocortisone (9a-fluorocorti-sol) is extremely potent and usually chosen for replacement mineralocorticoid therapy. In contrast, aldosterone and DOC are not useful in oral therapy due to rapid degradation in liver after absorption. [Pg.547]


See other pages where In liver is mentioned: [Pg.346]    [Pg.414]    [Pg.423]    [Pg.428]    [Pg.1058]    [Pg.399]    [Pg.309]    [Pg.32]    [Pg.229]    [Pg.474]    [Pg.597]    [Pg.601]    [Pg.616]    [Pg.748]    [Pg.753]    [Pg.754]    [Pg.760]    [Pg.760]    [Pg.798]    [Pg.821]    [Pg.849]    [Pg.164]    [Pg.286]    [Pg.1373]    [Pg.1080]    [Pg.56]    [Pg.73]    [Pg.119]    [Pg.190]    [Pg.216]    [Pg.257]    [Pg.323]    [Pg.495]    [Pg.496]    [Pg.497]    [Pg.538]    [Pg.548]   
See also in sourсe #XX -- [ Pg.18 , Pg.32 , Pg.44 ]

See also in sourсe #XX -- [ Pg.55 ]

See also in sourсe #XX -- [ Pg.455 , Pg.465 , Pg.467 ]




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8-Acetylharpagide activity in EBV, liver-1, lung

ALA synthetase in liver

Actions of growth hormone on protein synthesis in the liver

Ammonia in liver

Analysis ofp53 Mutations in Liver Cancer Patients

Assay of cholesterol 7a-hydroxylase in liver microsomes

Baccharis crispa in treatment of liver disease

Baccharis genistelloides in liver disorders

Baccharis genistelloides use in liver diseases

Blood in the liver

Butyltin concentrations in human liver

Cadmium in liver

Carcinogenesis in the Liver

Carcinogens in liver cultures

Cholesterol in the liver

Cholesterol, esterification, in liver

Copper accumulation in the liver

Copper in liver

Cytochrome P-450, in liver

Cytochrome in liver

D-Fructose in Liver, Intestine, and Kidney

Demethylation in liver

Distribution of Acid Phosphatase in Liver

Drug metabolism in liver

Effect of D-Fructose on the Nucleotide Pool in Liver

Effect of Lipotropic Substances on Phosphatide Turnover in Liver

Enzyme activity in liver

Fatty Liver and Kidney Syndrome in Biotin-Deficient hicks

Fatty acid in liver

Formation of alio bile acids in the liver

Fructose metabolism in liver

Glucagon in liver

Glucokinase in liver

Gluconeogenesis in liver

Glucose in liver

Glucose metabolism in liver

Glucose-6- phosphatase in liver

Glucuronidase in liver

Glucuronyl transferase in liver

Glutathione S-transferase developmental expression in liver

Glycogen content in rat liver

Glycogen metabolism in liver

Glycolysis in liver

Hepatoma, in the liver

Hypoalbuminemia in liver disease

In liver extracts

Induction in Liver and Intestine

Iron in liver

Ketogenesis in liver

Levels in human liver

Lipids in liver

Liver Specific Drug Transport in Sandwich-cultured Hepatocytes

Liver cells in vitro

Liver in Wilson’s disease

Liver in biosynthesis

Liver in vivo

Liver necrosis in rat

Liver tumors, in mice and rats

Mercury in liver

Metabolic zoning, in the liver

Metabolism in Liver Cultures

Metabolism in liver

Metastasis in liver

Metastatic tumor cells in liver

Metastatic tumor growth in liver

Mitochondria in liver

Mutations in Liver Tumours

Nitric oxide in liver disease

OCPs in cod liver oil

Pharmacokinetics of drugs in liver disease

Plasma Alpha-Class GST Measurements in Liver Disease

Regulation of lipogenesis in the liver

Relative Synthesis Rates in Liver Disease

Reperfusion Injury in Liver Allografts

Retinyl esters in liver

Selenium in liver

Silver in liver

Skin stigmata in liver disease

Studies with Isolated Liver Cells in Culture

Synergistic interaction between glucagon and calcium-mobilizing agonists in liver

Transport in Liver Slices

Triacylglycerols in liver

Triglycerides in the Liver

Turnover of Acid-Soluble Phosphorus in the Liver

Unscheduled DNA Synthesis Test in Liver Cells

Zinc in liver

Zoning in the Liver

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