Search PubMed⌕ Search

Biomedical subjects

W Gerok

Publications and source records attributed to W Gerok.

At least 343 records · Page 19Linked to original sources
PubMed1978

Induction and 'superinduction' of sialylation of membrane-bound gamma-glutamyltransferase during liver regeneration.

The present paper shows that in the regenerating rat liver the membrane-bound-gamma-glutamyltransferase exists in two molecular forms. Depending on the state of proliferation, a sialic-acid-rich enzyme (in the fetal or regenerating liver) or a sialic-acid-poor enzyme (in the adult or quiescent liver) could be detected. In regeneration liver (24 h after 2/3 resection) only the sialic-acid-rich or fetal enzyme could be found. Since total enzyme activity (adult + fetal type) remained unchanged, it is assumed that the adult type of gamma-glutamyltransferase was modified by sialylation during the initial phase of liver regeneration. This process of sialylation was prevented by inhibitors of RNA or protein synthesis such as D-galactosamine, actinomycin D or cycloheximide, provided that the inhibitor (D-galactosamine) was given within the first 8 h after partial hepatectomy. Sialylation was not impaired by inhibitors of DNA synthesis, e.g. hydroxyurea or cytosine arabinoside. Administration of actinomycin D during a defined phase of proliferation (24 to 48 h after partial hepatectomy) stimulated the transfer of sialic acid to gamma-glutamyltransferase, a finding which describes for the first time the so-called 'superinduction' of a sialylation process.

Animals↗
PubMed1978

Carbohydrate metabolism in renal failure.

Hyperglycemia and impaired glucose tolerance are well known phenomena occurring in patients with renal failure. In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Among the possible reasons, a disturbance at the cellular level seems to be most likely. There is some evidence of reduced peripheral glucose utilization on the one hand and increased hepatic glucose output--probably by stimulation of gluconeogenesis--on the other. Agents that have been suggested to be involved in these alterations of carbohydrate metabolism in uremia are hormones, electrolytes, pH, and "toxic" metabolic intermediates or end-products. Of these, an increase in insulin antagonistic hormones; among them growth hormone, catecholamines, and glucagon, seems to be of most significance. Although for the individual hormones no equivocal correlation with glucose intolerance has been proved, the interaction of all of them may result in a preponderance of insulin antagonism thus leading to an apparent insulin resistance.

Adrenal Glands↗
PubMed1978

[Determination of bile acids by radioimmunoassays (author's transl)].

The present paper, based on the current literature, considers the practical aspects of bile acid radioimmunoassays. The problems associated with the raising of specific antisera and their characterization are discussed. Features of assay design for bile acids are considered. Solid-phase radioimmunoassays are described for separate determination of unconjugated cholic acid and conjugated cholic acid in serum. The clinical application of specific bile acid radioimmunoassays is shown by an "oral cholate tolerance test" as a sensitive indicator of liver function and by an "oral cholylglycine tolerance test" for characterization of intestinal function in diarrheal states.

Bile Acids and Salts↗
PubMed1977

[New aspects of clinical hepatology (author's transl)].

Studies of the enzymes participating in the urea cycle and urine synthesis in the liver punctate show that typical changes occur in the enzyme pattern during chronic liver diseases which yield new starting points for the diagnostic classification and prognostic assessment. From studies on the metabolism of the bile acids it appears that, among the conditions for cholestasis, a fetal snythetic pathway for the bile acids with primary side chain oxidation of the cholesterol is followed, and intrahepatic monohydroxy-bile acids are formed. The pathogenetic significance of these bile acids for cholestasis is discussed.

Argininosuccinate Synthase↗
PubMed1977

[Biochemical and pathophysiological aspects of hyperammonaemia (author's transl)].

1. Ammonia liberated continuously in large amounts in muscle, kidney and brain is used immediately for the synthesis of mainly glutamine because of the toxic effects of elevated ammonia concentrations. After glutamine hydrolysis in the liver ammonia serves as substrate for the urea biosynthesis. In ureotelic animals urea is the quantitatively most important product for the elimination of surplus nitrogen. 2. The rate of urea biosynthesis depends on the amount of surplus nitrogen and acts as regulatory factor for the nitrogen balance of the adult organism. 3. Urea cycle abnormalities in liver diseases or inborn enzymatic defects are important factors leading to hyperammonaemia in patients. 4. The hyperammonaemia induces an increase of the rate of hepatic pyrimidine nucleotide biosynthesis as a consequence of an ineffective feedback inhibition of the glutamine-dependent carbamoyl phosphate synthetase. 5. The distribution of ammonia between intra- and extracellular space and the amount of ammonium ions excreted in the urine depend on the pH value. An alkalosis induces an intracellular ammonia load and inhibits the urinary ammonium ion excretion, which is increased in acidosis as one mechanism of protein elimination. 6. The ammonia-induced inhibition of the citric acid cycle by an alpha-ketoglutarate deficiency is one important reason for the neurotoxicity of ammonia, which is the main point in the pathogenesis of hepatic coma.

Ammonia↗
PubMed1977

Possible sites of interaction of acute renal failure with amino acid utilization for gluconeogenesis in isolated perfused rat liver.

Experiments were performed to elucidate the mechanisms involved in the enhanced conversion of amino acids to glucose in acute uraemic rats. Increased gluconeogenesis from a mixture of serine, threonine, lysine, glutamate, ornithine and citrulline was confirmed using a non-recirculating perfusion system. Stimulation was concentration dependent, being most pronounced at physiological amino acid concentrations. Stimulation of glucose and urea formation could be mimicked by using serine alone whereas with lactate and pyruvate inhibition of gluconeogenesis was observed. Serine dehydratase activity was significantly elevated following nephrectomy. Further, the uptake of the non-metabolize amino acid alpha-aminoisobutyrate was considerably increased. It is concluded that serine may play a special role as substrate for the additional glucose formation in acute uraemic rats, probably mediated by an activation of serine dehydratase. Acceleration of amino acid transport seems to represent an additional component of stimulation of amino acid utilization in acute uraemia.

Acute Kidney Injury↗
PubMed1977

Radioimmunoassay of serum-conjugated deoxycholic acid.

A specific, sensitive, and reliable radioimmunoassay for serum-conjugated deoxycholic acid has been developed with antiserum obtained after immunization of rabbits with deoxycholic acid--bovine serum albumin conjugate. The displacement curve of glyco [3H] deoxycholic acid was linear on a logit-log plot from 7.5 to 320 pmol of unlabeled glycodeoxycholic acid. At 50% displacement of bound label, the cross-reactivity of taurodeoxycholic acid was 100%, deoxycholic acid 30%, taurocholic acid 3%, and glycocholic acid 2%. No cross-reactivity was observed with free cholic acid, conjugated or free chenodeoxycholic acids and conjugated or free lithocholic acids. Fasting serum-conjugated deoxycholic acid concentrations in 10 healthy volunteers ranged from 0.18 to 0.92 mumol/1. Over a period of 5 hours following 0.5 g oral cholate administration the serum-conjugated deoxycholic acid concentration did not change in 5 fasting healthy persons, whereas an initial increase of serum cholic acid was observed.

Animals↗
PubMed1976

[Intracellular localisation of urea-cycle enzymes in liver (author's transl)].

Enzymes of the Krebs-Henseleit urea-cycle were localized by means of differential centrifugation and fractional tissue extraction in rat liver and in human liver. Argininosuccinatlyase (ASAL) and Argininosuccinatsynthetase (ASAS) represent enzymes of the soluble cytoplasmic fraction. Ornithine-ketoacid-transaminase(OKT), carbamyl-phosphate-synthetase (CPS) and ornithine-carbamyl-transferase (OCT) are localized in the mitochondrial and nuclei fractions of the liver cell. Most of the arginase activity is bound to subcellular structures (probably to nuclei). A small portion of arginase-activity was found in the soluble cytoplasmatic fraction. The enzymes of the Krebs-Henseleit urea-cycle are equally distributed in rat liver and in human liver. Differences in the subcellular localisation of (mitochondrial) enzymes in human liver could be attributed to mitochondrial breakage during tissue preparation and do not represent in-vivo conditions.

Animals↗
PubMed1976

Radioimmunoassay of serum conjugated cholic acid.

A radioimmunoassay for serum conjugated cholic acid is described using antiserum obtained five weeks after immunization of rabbits with cholic acid bovine serum albumin conjugate. Prior to the radioimmunoassay, extraction of bile acids was performed with Amberlite XAD-2. The displacement curve of glyco[3H]cholic acid was linear on a logit-log plot from 5 to 80 pmol of unlabelled glycocholic acid. Values for 8 normal fasting subjects ranged from 0.18 to 1.25 mumol/1. In 31 fasting subjects with or without liver disease serum values of conjugated cholic acid are related to serum bilirubin. Endoscopic retrograde cholangiopancreatography may influence serum levels of conjugated cholic acid.

Adult↗